---
_id: '9009'
abstract:
- lang: eng
text: Recent advancements in live cell imaging technologies have identified the
phenomenon of intracellular propagation of late apoptotic events, such as cytochrome
c release and caspase activation. The mechanism, prevalence, and speed of apoptosis
propagation remain unclear. Additionally, no studies have demonstrated propagation
of the pro-apoptotic protein, BAX. To evaluate the role of BAX in intracellular
apoptotic propagation, we used high speed live-cell imaging to visualize fluorescently
tagged-BAX recruitment to mitochondria in four immortalized cell lines. We show
that propagation of mitochondrial BAX recruitment occurs in parallel to cytochrome
c and SMAC/Diablo release and is affected by cellular morphology, such that cells
with processes are more likely to exhibit propagation. The initiation of propagation
events is most prevalent in the distal tips of processes, while the rate of propagation
is influenced by the 2-dimensional width of the process. Propagation was rarely
observed in the cell soma, which exhibited near synchronous recruitment of BAX.
Propagation velocity is not affected by mitochondrial volume in segments of processes,
but is negatively affected by mitochondrial density. There was no evidence of
a propagating wave of increased levels of intracellular calcium ions. Alternatively,
we did observe a uniform increase in superoxide build-up in cellular mitochondria,
which was released as a propagating wave simultaneously with the propagating recruitment
of BAX to the mitochondrial outer membrane.
acknowledgement: This work was supported by National Institute of Health grants R01
EY030123, P30 EY016665, and T32 GM081061, an unrestricted research grant from Research
to Prevent Blindness, Inc., and the Frederick A. Davis Endowment from the Department
of Ophthalmology and Visual Sciences at the University of Wisconsin-Madison.
article_processing_charge: No
article_type: original
author:
- first_name: Joshua A.
full_name: Grosser, Joshua A.
last_name: Grosser
- first_name: Margaret E
full_name: Maes, Margaret E
id: 3838F452-F248-11E8-B48F-1D18A9856A87
last_name: Maes
orcid: 0000-0001-9642-1085
- first_name: Robert W.
full_name: Nickells, Robert W.
last_name: Nickells
citation:
ama: Grosser JA, Maes ME, Nickells RW. Characteristics of intracellular propagation
of mitochondrial BAX recruitment during apoptosis. Apoptosis. 2021;26(2):132-145.
doi:10.1007/s10495-020-01654-w
apa: Grosser, J. A., Maes, M. E., & Nickells, R. W. (2021). Characteristics
of intracellular propagation of mitochondrial BAX recruitment during apoptosis.
Apoptosis. Springer Nature. https://doi.org/10.1007/s10495-020-01654-w
chicago: Grosser, Joshua A., Margaret E Maes, and Robert W. Nickells. “Characteristics
of Intracellular Propagation of Mitochondrial BAX Recruitment during Apoptosis.”
Apoptosis. Springer Nature, 2021. https://doi.org/10.1007/s10495-020-01654-w.
ieee: J. A. Grosser, M. E. Maes, and R. W. Nickells, “Characteristics of intracellular
propagation of mitochondrial BAX recruitment during apoptosis,” Apoptosis,
vol. 26, no. 2. Springer Nature, pp. 132–145, 2021.
ista: Grosser JA, Maes ME, Nickells RW. 2021. Characteristics of intracellular propagation
of mitochondrial BAX recruitment during apoptosis. Apoptosis. 26(2), 132–145.
mla: Grosser, Joshua A., et al. “Characteristics of Intracellular Propagation of
Mitochondrial BAX Recruitment during Apoptosis.” Apoptosis, vol. 26, no.
2, Springer Nature, 2021, pp. 132–45, doi:10.1007/s10495-020-01654-w.
short: J.A. Grosser, M.E. Maes, R.W. Nickells, Apoptosis 26 (2021) 132–145.
date_created: 2021-01-17T23:01:11Z
date_published: 2021-02-01T00:00:00Z
date_updated: 2023-08-07T13:32:40Z
day: '01'
department:
- _id: SaSi
doi: 10.1007/s10495-020-01654-w
external_id:
isi:
- '000606722600001'
pmid:
- '33426618'
fulldoi: https://doi.org/10.1007/s10495-020-01654-w
intvolume: ' 26'
isi: 1
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8082518/
month: '02'
oa: 1
oa_version: Submitted Version
page: 132-145
pmid: 1
publication: Apoptosis
publication_identifier:
eissn:
- 1573-675X
issn:
- 1360-8185
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Characteristics of intracellular propagation of mitochondrial BAX recruitment
during apoptosis
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 26
year: '2021'
...
---
_id: '9642'
abstract:
- lang: eng
text: Perineuronal nets (PNNs), components of the extracellular matrix, preferentially
coat parvalbumin-positive interneurons and constrain critical-period plasticity
in the adult cerebral cortex. Current strategies to remove PNN are long-lasting,
invasive, and trigger neuropsychiatric symptoms. Here, we apply repeated anesthetic
ketamine as a method with minimal behavioral effect. We find that this paradigm
strongly reduces PNN coating in the healthy adult brain and promotes juvenile-like
plasticity. Microglia are critically involved in PNN loss because they engage
with parvalbumin-positive neurons in their defined cortical layer. We identify
external 60-Hz light-flickering entrainment to recapitulate microglia-mediated
PNN removal. Importantly, 40-Hz frequency, which is known to remove amyloid plaques,
does not induce PNN loss, suggesting microglia might functionally tune to distinct
brain frequencies. Thus, our 60-Hz light-entrainment strategy provides an alternative
form of PNN intervention in the healthy adult brain.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: We thank the scientific service units at IST Austria, especially
the IST bioimaging facility, the preclinical facility, and, specifically, Michael
Schunn and Sonja Haslinger for excellent support; Plexxikon for the PLX food; the
Csicsvari group for advice and equipment for in vivo recording; Jürgen Siegert for
the light-entrainment design; Marco Benevento, Soledad Gonzalo Cogno, Pat King,
and all Siegert group members for constant feedback on the project and manuscript;
Lorena Pantano (PILM Bioinformatics Core) for assisting with sample-size determination
for OD plasticity experiments; and Ana Morello from MIT for technical assistance
with VEPs recordings. This research was supported by a DOC Fellowship from the Austrian
Academy of Sciences at the Institute of Science and Technology Austria to R.S.,
from the European Union Horizon 2020 research and innovation program under the Marie
Skłodowska-Curie Actions program (grants 665385 to G.C.; 754411 to R.J.A.C.), the
European Research Council (grant 715571 to S.S.), and the National Eye Institute
of the National Institutes of Health under award numbers R01EY029245 (to M.F.B.)
and R01EY023037 (diversity supplement to H.D.J-C.).
article_number: '109313'
article_processing_charge: No
article_type: original
author:
- first_name: Alessandro
full_name: Venturino, Alessandro
id: 41CB84B2-F248-11E8-B48F-1D18A9856A87
last_name: Venturino
orcid: 0000-0003-2356-9403
- first_name: Rouven
full_name: Schulz, Rouven
id: 4C5E7B96-F248-11E8-B48F-1D18A9856A87
last_name: Schulz
orcid: 0000-0001-5297-733X
- first_name: Héctor
full_name: De Jesús-Cortés, Héctor
last_name: De Jesús-Cortés
- first_name: Margaret E
full_name: Maes, Margaret E
id: 3838F452-F248-11E8-B48F-1D18A9856A87
last_name: Maes
orcid: 0000-0001-9642-1085
- first_name: Balint
full_name: Nagy, Balint
id: 93C65ECC-A6F2-11E9-8DF9-9712E6697425
last_name: Nagy
- first_name: Francis
full_name: Reilly-Andújar, Francis
last_name: Reilly-Andújar
- first_name: Gloria
full_name: Colombo, Gloria
id: 3483CF6C-F248-11E8-B48F-1D18A9856A87
last_name: Colombo
orcid: 0000-0001-9434-8902
- first_name: Ryan J
full_name: Cubero, Ryan J
id: 850B2E12-9CD4-11E9-837F-E719E6697425
last_name: Cubero
orcid: 0000-0003-0002-1867
- first_name: Florianne E
full_name: Schoot Uiterkamp, Florianne E
id: 3526230C-F248-11E8-B48F-1D18A9856A87
last_name: Schoot Uiterkamp
- first_name: Mark F.
full_name: Bear, Mark F.
last_name: Bear
- first_name: Sandra
full_name: Siegert, Sandra
id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
last_name: Siegert
orcid: 0000-0001-8635-0877
citation:
ama: Venturino A, Schulz R, De Jesús-Cortés H, et al. Microglia enable mature perineuronal
nets disassembly upon anesthetic ketamine exposure or 60-Hz light entrainment
in the healthy brain. Cell Reports. 2021;36(1). doi:10.1016/j.celrep.2021.109313
apa: Venturino, A., Schulz, R., De Jesús-Cortés, H., Maes, M. E., Nagy, B., Reilly-Andújar,
F., … Siegert, S. (2021). Microglia enable mature perineuronal nets disassembly
upon anesthetic ketamine exposure or 60-Hz light entrainment in the healthy brain.
Cell Reports. Elsevier. https://doi.org/10.1016/j.celrep.2021.109313
chicago: Venturino, Alessandro, Rouven Schulz, Héctor De Jesús-Cortés, Margaret
E Maes, Balint Nagy, Francis Reilly-Andújar, Gloria Colombo, et al. “Microglia
Enable Mature Perineuronal Nets Disassembly upon Anesthetic Ketamine Exposure
or 60-Hz Light Entrainment in the Healthy Brain.” Cell Reports. Elsevier,
2021. https://doi.org/10.1016/j.celrep.2021.109313.
ieee: A. Venturino et al., “Microglia enable mature perineuronal nets disassembly
upon anesthetic ketamine exposure or 60-Hz light entrainment in the healthy brain,”
Cell Reports, vol. 36, no. 1. Elsevier, 2021.
ista: Venturino A, Schulz R, De Jesús-Cortés H, Maes ME, Nagy B, Reilly-Andújar
F, Colombo G, Cubero RJ, Miteva FE, Bear MF, Siegert S. 2021. Microglia enable
mature perineuronal nets disassembly upon anesthetic ketamine exposure or 60-Hz
light entrainment in the healthy brain. Cell Reports. 36(1), 109313.
mla: Venturino, Alessandro, et al. “Microglia Enable Mature Perineuronal Nets Disassembly
upon Anesthetic Ketamine Exposure or 60-Hz Light Entrainment in the Healthy Brain.”
Cell Reports, vol. 36, no. 1, 109313, Elsevier, 2021, doi:10.1016/j.celrep.2021.109313.
short: A. Venturino, R. Schulz, H. De Jesús-Cortés, M.E. Maes, B. Nagy, F. Reilly-Andújar,
G. Colombo, R.J. Cubero, F.E. Miteva, M.F. Bear, S. Siegert, Cell Reports 36 (2021).
date_created: 2021-07-11T22:01:16Z
date_published: 2021-07-06T00:00:00Z
date_updated: 2026-04-03T09:46:05Z
day: '06'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1016/j.celrep.2021.109313
ec_funded: 1
external_id:
isi:
- '000670188500004'
pmid:
- '34233180'
file:
- access_level: open_access
checksum: f056255f6d01fd9a86b5387635928173
content_type: application/pdf
creator: cziletti
date_created: 2021-07-19T13:32:17Z
date_updated: 2021-07-19T13:32:17Z
file_id: '9693'
file_name: 2021_CellReports_Venturino.pdf
file_size: 56388540
relation: main_file
success: 1
file_date_updated: 2021-07-19T13:32:17Z
fulldoi: https://doi.org/10.1016/j.celrep.2021.109313
has_accepted_license: '1'
intvolume: ' 36'
isi: 1
issue: '1'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 25D4A630-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '715571'
name: Microglia action towards neuronal circuit formation and function in health
and disease
publication: Cell Reports
publication_identifier:
eissn:
- 2211-1247
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/the-twinkle-and-the-brain/
scopus_import: '1'
status: public
title: Microglia enable mature perineuronal nets disassembly upon anesthetic ketamine
exposure or 60-Hz light entrainment in the healthy brain
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 36
year: '2021'
...
---
_id: '9761'
abstract:
- lang: eng
text: 'The important roles of mitochondrial function and dysfunction in the process
of neurodegeneration are widely acknowledged. Retinal ganglion cells (RGCs) appear
to be a highly vulnerable neuronal cell type in the central nervous system with
respect to mitochondrial dysfunction but the actual reasons for this are still
incompletely understood. These cells have a unique circumstance where unmyelinated
axons must bend nearly 90° to exit the eye and then cross a translaminar pressure
gradient before becoming myelinated in the optic nerve. This region, the optic
nerve head, contains some of the highest density of mitochondria present in these
cells. Glaucoma represents a perfect storm of events occurring at this location,
with a combination of changes in the translaminar pressure gradient and reassignment
of the metabolic support functions of supporting glia, which appears to apply
increased metabolic stress to the RGC axons leading to a failure of axonal transport
mechanisms. However, RGCs themselves are also extremely sensitive to genetic mutations,
particularly in genes affecting mitochondrial dynamics and mitochondrial clearance.
These mutations, which systemically affect the mitochondria in every cell, often
lead to an optic neuropathy as the sole pathologic defect in affected patients.
This review summarizes knowledge of mitochondrial structure and function, the
known energy demands of neurons in general, and places these in the context of
normal and pathological characteristics of mitochondria attributed to RGCs. '
acknowledgement: The authors are grateful to Kazuya Oikawa and Gillian McLellan for
generously sharing some of their data for this review, and to Janis Eells for helpful
comments on the manuscript.
article_number: '1593'
article_processing_charge: Yes
article_type: original
author:
- first_name: Nicole A.
full_name: Muench, Nicole A.
last_name: Muench
- first_name: Sonia
full_name: Patel, Sonia
last_name: Patel
- first_name: Margaret E
full_name: Maes, Margaret E
id: 3838F452-F248-11E8-B48F-1D18A9856A87
last_name: Maes
orcid: 0000-0001-9642-1085
- first_name: Ryan J.
full_name: Donahue, Ryan J.
last_name: Donahue
- first_name: Akihiro
full_name: Ikeda, Akihiro
last_name: Ikeda
- first_name: Robert W.
full_name: Nickells, Robert W.
last_name: Nickells
citation:
ama: Muench NA, Patel S, Maes ME, Donahue RJ, Ikeda A, Nickells RW. The influence
of mitochondrial dynamics and function on retinal ganglion cell susceptibility
in optic nerve disease. Cells. 2021;10(7). doi:10.3390/cells10071593
apa: Muench, N. A., Patel, S., Maes, M. E., Donahue, R. J., Ikeda, A., & Nickells,
R. W. (2021). The influence of mitochondrial dynamics and function on retinal
ganglion cell susceptibility in optic nerve disease. Cells. MDPI. https://doi.org/10.3390/cells10071593
chicago: Muench, Nicole A., Sonia Patel, Margaret E Maes, Ryan J. Donahue, Akihiro
Ikeda, and Robert W. Nickells. “The Influence of Mitochondrial Dynamics and Function
on Retinal Ganglion Cell Susceptibility in Optic Nerve Disease.” Cells.
MDPI, 2021. https://doi.org/10.3390/cells10071593.
ieee: N. A. Muench, S. Patel, M. E. Maes, R. J. Donahue, A. Ikeda, and R. W. Nickells,
“The influence of mitochondrial dynamics and function on retinal ganglion cell
susceptibility in optic nerve disease,” Cells, vol. 10, no. 7. MDPI, 2021.
ista: Muench NA, Patel S, Maes ME, Donahue RJ, Ikeda A, Nickells RW. 2021. The influence
of mitochondrial dynamics and function on retinal ganglion cell susceptibility
in optic nerve disease. Cells. 10(7), 1593.
mla: Muench, Nicole A., et al. “The Influence of Mitochondrial Dynamics and Function
on Retinal Ganglion Cell Susceptibility in Optic Nerve Disease.” Cells,
vol. 10, no. 7, 1593, MDPI, 2021, doi:10.3390/cells10071593.
short: N.A. Muench, S. Patel, M.E. Maes, R.J. Donahue, A. Ikeda, R.W. Nickells,
Cells 10 (2021).
date_created: 2021-08-01T22:01:22Z
date_published: 2021-06-25T00:00:00Z
date_updated: 2026-04-02T13:56:24Z
day: '25'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.3390/cells10071593
external_id:
isi:
- '000678193300001'
pmid:
- '34201955'
file:
- access_level: open_access
checksum: e0497ce5c77fa3b65a538c7d6e0f6c66
content_type: application/pdf
creator: cziletti
date_created: 2021-08-04T14:01:30Z
date_updated: 2021-08-04T14:01:30Z
file_id: '9768'
file_name: 2021_Cells_Muench.pdf
file_size: 4555611
relation: main_file
success: 1
file_date_updated: 2021-08-04T14:01:30Z
fulldoi: https://doi.org/10.3390/cells10071593
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
issue: '7'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: Cells
publication_identifier:
eissn:
- 2073-4409
publication_status: published
publisher: MDPI
quality_controlled: '1'
scopus_import: '1'
status: public
title: The influence of mitochondrial dynamics and function on retinal ganglion cell
susceptibility in optic nerve disease
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 10
year: '2021'
...
---
_id: '9874'
abstract:
- lang: eng
text: Myocardial regeneration is restricted to early postnatal life, when mammalian
cardiomyocytes still retain the ability to proliferate. The molecular cues that
induce cell cycle arrest of neonatal cardiomyocytes towards terminally differentiated
adult heart muscle cells remain obscure. Here we report that the miR-106b~25 cluster
is higher expressed in the early postnatal myocardium and decreases in expression
towards adulthood, especially under conditions of overload, and orchestrates the
transition of cardiomyocyte hyperplasia towards cell cycle arrest and hypertrophy
by virtue of its targetome. In line, gene delivery of miR-106b~25 to the mouse
heart provokes cardiomyocyte proliferation by targeting a network of negative
cell cycle regulators including E2f5, Cdkn1c, Ccne1 and Wee1. Conversely, gene-targeted
miR-106b~25 null mice display spontaneous hypertrophic remodeling and exaggerated
remodeling to overload by derepression of the prohypertrophic transcription factors
Hand2 and Mef2d. Taking advantage of the regulatory function of miR-106b~25 on
cardiomyocyte hyperplasia and hypertrophy, viral gene delivery of miR-106b~25
provokes nearly complete regeneration of the adult myocardium after ischemic injury.
Our data demonstrate that exploitation of conserved molecular programs can enhance
the regenerative capacity of the injured heart.
acknowledgement: E.D. is supported by a VENI award 916-150-16 from the Netherlands
Organization for Health Research and Development (ZonMW), an EMBO Long-term Fellowship
(EMBO ALTF 848-2013) and a FP7 Marie Curie Intra-European Fellowship (Project number
627539). V.S.P. was funded by a fellowship from the FCT/ Ministério da Ciência,
Tecnologia e Inovação SFRH/BD/111799/2015. P.D.C.M. is an Established Investigator
of the Dutch Heart Foundation. L.D.W. acknowledges support from the Dutch CardioVascular
Alliance (ARENA-PRIME). L.D.W. was further supported by grant 311549 from the European
Research Council (ERC), a VICI award 918-156-47 from the Dutch Research Council
and Marie Sklodowska-Curie grant agreement no. 813716 (TRAIN-HEART).
article_number: '4808'
article_processing_charge: Yes
article_type: original
author:
- first_name: Andrea
full_name: Raso, Andrea
last_name: Raso
- first_name: Ellen
full_name: Dirkx, Ellen
last_name: Dirkx
- first_name: Vasco
full_name: Sampaio-Pinto, Vasco
last_name: Sampaio-Pinto
- first_name: Hamid
full_name: el Azzouzi, Hamid
last_name: el Azzouzi
- first_name: Ryan J
full_name: Cubero, Ryan J
id: 850B2E12-9CD4-11E9-837F-E719E6697425
last_name: Cubero
orcid: 0000-0003-0002-1867
- first_name: Daniel W.
full_name: Sorensen, Daniel W.
last_name: Sorensen
- first_name: Lara
full_name: Ottaviani, Lara
last_name: Ottaviani
- first_name: Servé
full_name: Olieslagers, Servé
last_name: Olieslagers
- first_name: Manon M.
full_name: Huibers, Manon M.
last_name: Huibers
- first_name: Roel
full_name: de Weger, Roel
last_name: de Weger
- first_name: Sailay
full_name: Siddiqi, Sailay
last_name: Siddiqi
- first_name: Silvia
full_name: Moimas, Silvia
last_name: Moimas
- first_name: Consuelo
full_name: Torrini, Consuelo
last_name: Torrini
- first_name: Lorena
full_name: Zentillin, Lorena
last_name: Zentillin
- first_name: Luca
full_name: Braga, Luca
last_name: Braga
- first_name: Diana S.
full_name: Nascimento, Diana S.
last_name: Nascimento
- first_name: Paula A.
full_name: da Costa Martins, Paula A.
last_name: da Costa Martins
- first_name: Jop H.
full_name: van Berlo, Jop H.
last_name: van Berlo
- first_name: Serena
full_name: Zacchigna, Serena
last_name: Zacchigna
- first_name: Mauro
full_name: Giacca, Mauro
last_name: Giacca
- first_name: Leon J.
full_name: De Windt, Leon J.
last_name: De Windt
citation:
ama: Raso A, Dirkx E, Sampaio-Pinto V, et al. A microRNA program regulates the balance
between cardiomyocyte hyperplasia and hypertrophy and stimulates cardiac regeneration.
Nature Communications. 2021;12. doi:10.1038/s41467-021-25211-4
apa: Raso, A., Dirkx, E., Sampaio-Pinto, V., el Azzouzi, H., Cubero, R. J., Sorensen,
D. W., … De Windt, L. J. (2021). A microRNA program regulates the balance between
cardiomyocyte hyperplasia and hypertrophy and stimulates cardiac regeneration.
Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-021-25211-4
chicago: Raso, Andrea, Ellen Dirkx, Vasco Sampaio-Pinto, Hamid el Azzouzi, Ryan
J Cubero, Daniel W. Sorensen, Lara Ottaviani, et al. “A MicroRNA Program Regulates
the Balance between Cardiomyocyte Hyperplasia and Hypertrophy and Stimulates Cardiac
Regeneration.” Nature Communications. Springer Nature, 2021. https://doi.org/10.1038/s41467-021-25211-4.
ieee: A. Raso et al., “A microRNA program regulates the balance between cardiomyocyte
hyperplasia and hypertrophy and stimulates cardiac regeneration,” Nature Communications,
vol. 12. Springer Nature, 2021.
ista: Raso A, Dirkx E, Sampaio-Pinto V, el Azzouzi H, Cubero RJ, Sorensen DW, Ottaviani
L, Olieslagers S, Huibers MM, de Weger R, Siddiqi S, Moimas S, Torrini C, Zentillin
L, Braga L, Nascimento DS, da Costa Martins PA, van Berlo JH, Zacchigna S, Giacca
M, De Windt LJ. 2021. A microRNA program regulates the balance between cardiomyocyte
hyperplasia and hypertrophy and stimulates cardiac regeneration. Nature Communications.
12, 4808.
mla: Raso, Andrea, et al. “A MicroRNA Program Regulates the Balance between Cardiomyocyte
Hyperplasia and Hypertrophy and Stimulates Cardiac Regeneration.” Nature Communications,
vol. 12, 4808, Springer Nature, 2021, doi:10.1038/s41467-021-25211-4.
short: A. Raso, E. Dirkx, V. Sampaio-Pinto, H. el Azzouzi, R.J. Cubero, D.W. Sorensen,
L. Ottaviani, S. Olieslagers, M.M. Huibers, R. de Weger, S. Siddiqi, S. Moimas,
C. Torrini, L. Zentillin, L. Braga, D.S. Nascimento, P.A. da Costa Martins, J.H.
van Berlo, S. Zacchigna, M. Giacca, L.J. De Windt, Nature Communications 12 (2021).
date_created: 2021-08-10T11:49:20Z
date_published: 2021-08-10T00:00:00Z
date_updated: 2023-08-11T10:27:03Z
day: '10'
ddc:
- '610'
- '570'
department:
- _id: SaSi
doi: 10.1038/s41467-021-25211-4
external_id:
isi:
- '000683910200042'
pmid:
- '34376683'
file:
- access_level: open_access
checksum: 48d8562e8229e4282f3f354b329722c5
content_type: application/pdf
creator: asandaue
date_created: 2021-08-10T12:29:59Z
date_updated: 2021-08-10T12:29:59Z
file_id: '9876'
file_name: 2021_NatureCommunications_Raso.pdf
file_size: 4364333
relation: main_file
success: 1
file_date_updated: 2021-08-10T12:29:59Z
fulldoi: https://doi.org/10.1038/s41467-021-25211-4
genbank:
- GSE178867
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1038/s41467-022-32785-0
scopus_import: '1'
status: public
title: A microRNA program regulates the balance between cardiomyocyte hyperplasia
and hypertrophy and stimulates cardiac regeneration
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '10000'
abstract:
- lang: eng
text: Inhibition or targeted deletion of histone deacetylase 3 (HDAC3) is neuroprotective
in a variety neurodegenerative conditions, including retinal ganglion cells (RGCs)
after acute optic nerve damage. Consistent with this, induced HDAC3 expression
in cultured cells shows selective toxicity to neurons. Despite an established
role for HDAC3 in neuronal pathology, little is known regarding the mechanism
of this pathology.
acknowledgement: 'The authors thank Joel Dietz for maintaining the mice used in this
study, Satoshi Kinoshita and the Translational Research Initiative in Pathology
Laboratory at the University of Wisconsin-Madison for cutting retinal sections analyzed
in this study, and Mark Banghart for statistical review of the data analysis. Supported
by National Eye Institute Grants R01 EY012223 (RWN), R01 EY030123 (RWN), R01 EY029809
(LWG), R01 EY029809 (LWG) and a Vision Research CORE grant P30 EY016665, NRSA grant
T32 GM081061, by an unrestricted research grant from Research to Prevent Blindness,
Inc., and by a University of Wisconsin-Madison Vilas Life Cycle award and the Frederick
A. Davis Research Chair (RWN). '
article_number: '14'
article_processing_charge: Yes
article_type: original
author:
- first_name: Heather M.
full_name: Schmitt, Heather M.
last_name: Schmitt
- first_name: Rachel L.
full_name: Fehrman, Rachel L.
last_name: Fehrman
- first_name: Margaret E
full_name: Maes, Margaret E
id: 3838F452-F248-11E8-B48F-1D18A9856A87
last_name: Maes
orcid: 0000-0001-9642-1085
- first_name: Huan
full_name: Yang, Huan
last_name: Yang
- first_name: Lian Wang
full_name: Guo, Lian Wang
last_name: Guo
- first_name: Cassandra L.
full_name: Schlamp, Cassandra L.
last_name: Schlamp
- first_name: Heather R.
full_name: Pelzel, Heather R.
last_name: Pelzel
- first_name: Robert W.
full_name: Nickells, Robert W.
last_name: Nickells
citation:
ama: Schmitt HM, Fehrman RL, Maes ME, et al. Increased susceptibility and intrinsic
apoptotic signaling in neurons by induced HDAC3 expression. Investigative Ophthalmology
& Visual Science. 2021;62(10). doi:10.1167/IOVS.62.10.14
apa: Schmitt, H. M., Fehrman, R. L., Maes, M. E., Yang, H., Guo, L. W., Schlamp,
C. L., … Nickells, R. W. (2021). Increased susceptibility and intrinsic apoptotic
signaling in neurons by induced HDAC3 expression. Investigative Ophthalmology
& Visual Science. Association for Research in Vision and Ophthalmology.
https://doi.org/10.1167/IOVS.62.10.14
chicago: Schmitt, Heather M., Rachel L. Fehrman, Margaret E Maes, Huan Yang, Lian
Wang Guo, Cassandra L. Schlamp, Heather R. Pelzel, and Robert W. Nickells. “Increased
Susceptibility and Intrinsic Apoptotic Signaling in Neurons by Induced HDAC3 Expression.”
Investigative Ophthalmology & Visual Science. Association for Research
in Vision and Ophthalmology, 2021. https://doi.org/10.1167/IOVS.62.10.14.
ieee: H. M. Schmitt et al., “Increased susceptibility and intrinsic apoptotic
signaling in neurons by induced HDAC3 expression,” Investigative Ophthalmology
& Visual Science, vol. 62, no. 10. Association for Research in Vision
and Ophthalmology, 2021.
ista: Schmitt HM, Fehrman RL, Maes ME, Yang H, Guo LW, Schlamp CL, Pelzel HR, Nickells
RW. 2021. Increased susceptibility and intrinsic apoptotic signaling in neurons
by induced HDAC3 expression. Investigative Ophthalmology & Visual Science.
62(10), 14.
mla: Schmitt, Heather M., et al. “Increased Susceptibility and Intrinsic Apoptotic
Signaling in Neurons by Induced HDAC3 Expression.” Investigative Ophthalmology
& Visual Science, vol. 62, no. 10, 14, Association for Research in Vision
and Ophthalmology, 2021, doi:10.1167/IOVS.62.10.14.
short: H.M. Schmitt, R.L. Fehrman, M.E. Maes, H. Yang, L.W. Guo, C.L. Schlamp, H.R.
Pelzel, R.W. Nickells, Investigative Ophthalmology & Visual Science 62 (2021).
date_created: 2021-09-12T22:01:23Z
date_published: 2021-08-16T00:00:00Z
date_updated: 2026-08-12T11:15:05Z
day: '16'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1167/IOVS.62.10.14
external_id:
isi:
- '000695230000014'
pmid:
- '34398198'
file:
- access_level: open_access
checksum: c430967746f653aa1ae84ee617f62b73
content_type: application/pdf
creator: dernst
date_created: 2022-05-13T07:40:15Z
date_updated: 2022-05-13T07:40:15Z
file_id: '11369'
file_name: 2021_IOVS_Schmitt.pdf
file_size: 19707796
relation: main_file
success: 1
file_date_updated: 2022-05-13T07:40:15Z
fulldoi: https://doi.org/10.1167/IOVS.62.10.14
has_accepted_license: '1'
intvolume: ' 62'
isi: 1
issue: '10'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
publication: Investigative Ophthalmology & Visual Science
publication_identifier:
eissn:
- 1552-5783
issn:
- 0146-0404
publication_status: published
publisher: Association for Research in Vision and Ophthalmology
quality_controlled: '1'
scopus_import: '1'
status: public
title: Increased susceptibility and intrinsic apoptotic signaling in neurons by induced
HDAC3 expression
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 62
year: '2021'
...
---
_id: '7632'
abstract:
- lang: eng
text: The posterior parietal cortex (PPC) and frontal motor areas comprise a cortical
network supporting goal-directed behaviour, with functions including sensorimotor
transformations and decision making. In primates, this network links performed
and observed actions via mirror neurons, which fire both when individuals perform
an action and when they observe the same action performed by a conspecific. Mirror
neurons are believed to be important for social learning, but it is not known
whether mirror-like neurons occur in similar networks in other social species,
such as rodents, or if they can be measured in such models using paradigms where
observers passively view a demonstrator. Therefore, we imaged Ca2+ responses in
PPC and secondary motor cortex (M2) while mice performed and observed pellet-reaching
and wheel-running tasks, and found that cell populations in both areas robustly
encoded several naturalistic behaviours. However, neural responses to the same
set of observed actions were absent, although we verified that observer mice were
attentive to performers and that PPC neurons responded reliably to visual cues.
Statistical modelling also indicated that executed actions outperformed observed
actions in predicting neural responses. These results raise the possibility that
sensorimotor action recognition in rodents could take place outside of the parieto-frontal
circuit, and underscore that detecting socially-driven neural coding depends critically
on the species and behavioural paradigm used.
article_number: '5559'
article_processing_charge: No
article_type: original
author:
- first_name: Tuce
full_name: Tombaz, Tuce
last_name: Tombaz
- first_name: Benjamin A.
full_name: Dunn, Benjamin A.
last_name: Dunn
- first_name: Karoline
full_name: Hovde, Karoline
last_name: Hovde
- first_name: Ryan J
full_name: Cubero, Ryan J
id: 850B2E12-9CD4-11E9-837F-E719E6697425
last_name: Cubero
orcid: 0000-0003-0002-1867
- first_name: Bartul
full_name: Mimica, Bartul
last_name: Mimica
- first_name: Pranav
full_name: Mamidanna, Pranav
last_name: Mamidanna
- first_name: Yasser
full_name: Roudi, Yasser
last_name: Roudi
- first_name: Jonathan R.
full_name: Whitlock, Jonathan R.
last_name: Whitlock
citation:
ama: Tombaz T, Dunn BA, Hovde K, et al. Action representation in the mouse parieto-frontal
network. Scientific reports. 2020;10(1). doi:10.1038/s41598-020-62089-6
apa: Tombaz, T., Dunn, B. A., Hovde, K., Cubero, R. J., Mimica, B., Mamidanna, P.,
… Whitlock, J. R. (2020). Action representation in the mouse parieto-frontal network.
Scientific Reports. Springer Nature. https://doi.org/10.1038/s41598-020-62089-6
chicago: Tombaz, Tuce, Benjamin A. Dunn, Karoline Hovde, Ryan J Cubero, Bartul Mimica,
Pranav Mamidanna, Yasser Roudi, and Jonathan R. Whitlock. “Action Representation
in the Mouse Parieto-Frontal Network.” Scientific Reports. Springer Nature,
2020. https://doi.org/10.1038/s41598-020-62089-6.
ieee: T. Tombaz et al., “Action representation in the mouse parieto-frontal
network,” Scientific reports, vol. 10, no. 1. Springer Nature, 2020.
ista: Tombaz T, Dunn BA, Hovde K, Cubero RJ, Mimica B, Mamidanna P, Roudi Y, Whitlock
JR. 2020. Action representation in the mouse parieto-frontal network. Scientific
reports. 10(1), 5559.
mla: Tombaz, Tuce, et al. “Action Representation in the Mouse Parieto-Frontal Network.”
Scientific Reports, vol. 10, no. 1, 5559, Springer Nature, 2020, doi:10.1038/s41598-020-62089-6.
short: T. Tombaz, B.A. Dunn, K. Hovde, R.J. Cubero, B. Mimica, P. Mamidanna, Y.
Roudi, J.R. Whitlock, Scientific Reports 10 (2020).
date_created: 2020-04-05T22:00:47Z
date_published: 2020-03-27T00:00:00Z
date_updated: 2026-04-02T14:23:52Z
day: '27'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1038/s41598-020-62089-6
external_id:
isi:
- '000560406800007'
file:
- access_level: open_access
checksum: e6cfaaaf7986532132934400038b824a
content_type: application/pdf
creator: dernst
date_created: 2020-04-06T10:44:23Z
date_updated: 2020-07-14T12:48:01Z
file_id: '7644'
file_name: 2020_ScientificReports_Tombaz.pdf
file_size: 2621249
relation: main_file
file_date_updated: 2020-07-14T12:48:01Z
fulldoi: https://doi.org/10.1038/s41598-020-62089-6
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
issue: '1'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: Scientific reports
publication_identifier:
eissn:
- 2045-2322
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Action representation in the mouse parieto-frontal network
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 10
year: '2020'
...
---
_id: '7880'
abstract:
- lang: eng
text: 'Following its evoked release, dopamine (DA) signaling is rapidly terminated
by presynaptic reuptake, mediated by the cocaine-sensitive DA transporter (DAT).
DAT surface availability is dynamically regulated by endocytic trafficking, and
direct protein kinase C (PKC) activation acutely diminishes DAT surface expression
by accelerating DAT internalization. Previous cell line studies demonstrated that
PKC-stimulated DAT endocytosis requires both Ack1 inactivation, which releases
a DAT-specific endocytic brake, and the neuronal GTPase, Rit2, which binds DAT.
However, it is unknown whether Rit2 is required for PKC-stimulated DAT endocytosis
in DAergic terminals or whether there are region- and/or sex-dependent differences
in PKC-stimulated DAT trafficking. Moreover, the mechanisms by which Rit2 controls
PKC-stimulated DAT endocytosis are unknown. Here, we directly examined these important
questions. Ex vivo studies revealed that PKC activation acutely decreased DAT
surface expression selectively in ventral, but not dorsal, striatum. AAV-mediated,
conditional Rit2 knockdown in DAergic neurons impacted baseline DAT surface:intracellular
distribution in DAergic terminals from female ventral, but not dorsal, striatum.
Further, Rit2 was required for PKC-stimulated DAT internalization in both male
and female ventral striatum. FRET and surface pulldown studies in cell lines revealed
that PKC activation drives DAT-Rit2 surface dissociation and that the DAT N terminus
is required for both PKC-mediated DAT-Rit2 dissociation and DAT internalization.
Finally, we found that Rit2 and Ack1 independently converge on DAT to facilitate
PKC-stimulated DAT endocytosis. Together, our data provide greater insight into
mechanisms that mediate PKC-regulated DAT internalization and reveal unexpected
region-specific differences in PKC-stimulated DAT trafficking in bona fide DAergic
terminals. '
article_processing_charge: No
article_type: original
author:
- first_name: Rita R.
full_name: Fagan, Rita R.
last_name: Fagan
- first_name: Patrick J.
full_name: Kearney, Patrick J.
last_name: Kearney
- first_name: Carolyn G.
full_name: Sweeney, Carolyn G.
last_name: Sweeney
- first_name: Dino
full_name: Luethi, Dino
last_name: Luethi
- first_name: Florianne E
full_name: Schoot Uiterkamp, Florianne E
id: 3526230C-F248-11E8-B48F-1D18A9856A87
last_name: Schoot Uiterkamp
- first_name: Klaus
full_name: Schicker, Klaus
last_name: Schicker
- first_name: Brian S.
full_name: Alejandro, Brian S.
last_name: Alejandro
- first_name: Lauren C.
full_name: O'Connor, Lauren C.
last_name: O'Connor
- first_name: Harald H.
full_name: Sitte, Harald H.
last_name: Sitte
- first_name: Haley E.
full_name: Melikian, Haley E.
last_name: Melikian
citation:
ama: 'Fagan RR, Kearney PJ, Sweeney CG, et al. Dopamine transporter trafficking
and Rit2 GTPase: Mechanism of action and in vivo impact. Journal of Biological
Chemistry. 2020;295(16):5229-5244. doi:10.1074/jbc.RA120.012628'
apa: 'Fagan, R. R., Kearney, P. J., Sweeney, C. G., Luethi, D., Schoot Uiterkamp,
F. E., Schicker, K., … Melikian, H. E. (2020). Dopamine transporter trafficking
and Rit2 GTPase: Mechanism of action and in vivo impact. Journal of Biological
Chemistry. ASBMB Publications. https://doi.org/10.1074/jbc.RA120.012628'
chicago: 'Fagan, Rita R., Patrick J. Kearney, Carolyn G. Sweeney, Dino Luethi, Florianne
E Schoot Uiterkamp, Klaus Schicker, Brian S. Alejandro, Lauren C. O’Connor, Harald
H. Sitte, and Haley E. Melikian. “Dopamine Transporter Trafficking and Rit2 GTPase:
Mechanism of Action and in Vivo Impact.” Journal of Biological Chemistry.
ASBMB Publications, 2020. https://doi.org/10.1074/jbc.RA120.012628.'
ieee: 'R. R. Fagan et al., “Dopamine transporter trafficking and Rit2 GTPase:
Mechanism of action and in vivo impact,” Journal of Biological Chemistry,
vol. 295, no. 16. ASBMB Publications, pp. 5229–5244, 2020.'
ista: 'Fagan RR, Kearney PJ, Sweeney CG, Luethi D, Schoot Uiterkamp FE, Schicker
K, Alejandro BS, O’Connor LC, Sitte HH, Melikian HE. 2020. Dopamine transporter
trafficking and Rit2 GTPase: Mechanism of action and in vivo impact. Journal of
Biological Chemistry. 295(16), 5229–5244.'
mla: 'Fagan, Rita R., et al. “Dopamine Transporter Trafficking and Rit2 GTPase:
Mechanism of Action and in Vivo Impact.” Journal of Biological Chemistry,
vol. 295, no. 16, ASBMB Publications, 2020, pp. 5229–44, doi:10.1074/jbc.RA120.012628.'
short: R.R. Fagan, P.J. Kearney, C.G. Sweeney, D. Luethi, F.E. Schoot Uiterkamp,
K. Schicker, B.S. Alejandro, L.C. O’Connor, H.H. Sitte, H.E. Melikian, Journal
of Biological Chemistry 295 (2020) 5229–5244.
date_created: 2020-05-24T22:00:59Z
date_published: 2020-04-17T00:00:00Z
date_updated: 2025-07-10T11:54:48Z
day: '17'
department:
- _id: SaSi
doi: 10.1074/jbc.RA120.012628
external_id:
isi:
- '000530288000006'
pmid:
- '32132171'
fulldoi: https://doi.org/10.1074/jbc.RA120.012628
intvolume: ' 295'
isi: 1
issue: '16'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://escholarship.umassmed.edu/oapubs/4187
month: '04'
oa: 1
oa_version: Submitted Version
page: 5229-5244
pmid: 1
publication: Journal of Biological Chemistry
publication_identifier:
eissn:
- 1083-351X
issn:
- 0021-9258
publication_status: published
publisher: ASBMB Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Dopamine transporter trafficking and Rit2 GTPase: Mechanism of action and
in vivo impact'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 295
year: '2020'
...
---
_id: '7033'
abstract:
- lang: eng
text: Removal of the Bax gene from mice completely protects the somas of retinal
ganglion cells (RGCs) from apoptosis following optic nerve injury. This makes
BAX a promising therapeutic target to prevent neurodegeneration. In this study,
Bax+/− mice were used to test the hypothesis that lowering the quantity of BAX
in RGCs would delay apoptosis following optic nerve injury. RGCs were damaged
by performing optic nerve crush (ONC) and then immunostaining for phospho-cJUN,
and quantitative PCR were used to monitor the status of the BAX activation mechanism
in the months following injury. The apoptotic susceptibility of injured cells
was directly tested by virally introducing GFP-BAX into Bax−/− RGCs after injury.
The competency of quiescent RGCs to reactivate their BAX activation mechanism
was tested by intravitreal injection of the JNK pathway agonist, anisomycin. Twenty-four
weeks after ONC, Bax+/− mice had significantly less cell loss in their RGC layer
than Bax+/+ mice 3 weeks after ONC. Bax+/− and Bax+/+ RGCs exhibited similar patterns
of nuclear phospho-cJUN accumulation immediately after ONC, which persisted in
Bax+/− RGCs for up to 7 weeks before abating. The transcriptional activation of
BAX-activating genes was similar in Bax+/− and Bax+/+ RGCs following ONC. Intriguingly,
cells deactivated their BAX activation mechanism between 7 and 12 weeks after
crush. Introduction of GFP-BAX into Bax−/− cells at 4 weeks after ONC showed that
these cells had a nearly normal capacity to activate this protein, but this capacity
was lost 8 weeks after crush. Collectively, these data suggest that 8–12 weeks
after crush, damaged cells no longer displayed increased susceptibility to BAX
activation relative to their naïve counterparts. In this same timeframe, retinal
glial activation and the signaling of the pro-apoptotic JNK pathway also abated.
Quiescent RGCs did not show a timely reactivation of their JNK pathway following
intravitreal injection with anisomycin. These findings demonstrate that lowering
the quantity of BAX in RGCs is neuroprotective after acute injury. Damaged RGCs
enter a quiescent state months after injury and are no longer responsive to an
apoptotic stimulus. Quiescent RGCs will require rejuvenation to reacquire functionality.
acknowledgement: This work was supported by National Eye Institute grants R01 EY012223
(RWN), R01 EY030123 (RWN), T32 EY027721 (Department of Ophthalmology and Visual
Sciences, University of Wisconsin-Madison), and a Vision Science Core grant P30
EY016665 (Department of Ophthalmology and Visual Sciences, University of Wisconsin-Madison),
an unrestricted funding grant from Research to Prevent Blindness (Department of
Ophthalmology and Visual Sciences, University of Wisconsin-Madison), the Frederick
A. Davis Endowment (RWN), and the Mr. and Mrs. George Taylor Foundation (RWN).
article_processing_charge: No
article_type: original
author:
- first_name: RJ
full_name: Donahue, RJ
last_name: Donahue
- first_name: Margaret E
full_name: Maes, Margaret E
id: 3838F452-F248-11E8-B48F-1D18A9856A87
last_name: Maes
orcid: 0000-0001-9642-1085
- first_name: JA
full_name: Grosser, JA
last_name: Grosser
- first_name: RW
full_name: Nickells, RW
last_name: Nickells
citation:
ama: Donahue R, Maes ME, Grosser J, Nickells R. BAX-depleted retinal ganglion cells
survive and become quiescent following optic nerve damage. Molecular Neurobiology.
2020;57(2):1070–1084. doi:10.1007/s12035-019-01783-7
apa: Donahue, R., Maes, M. E., Grosser, J., & Nickells, R. (2020). BAX-depleted
retinal ganglion cells survive and become quiescent following optic nerve damage.
Molecular Neurobiology. Springer Nature. https://doi.org/10.1007/s12035-019-01783-7
chicago: Donahue, RJ, Margaret E Maes, JA Grosser, and RW Nickells. “BAX-Depleted
Retinal Ganglion Cells Survive and Become Quiescent Following Optic Nerve Damage.”
Molecular Neurobiology. Springer Nature, 2020. https://doi.org/10.1007/s12035-019-01783-7.
ieee: R. Donahue, M. E. Maes, J. Grosser, and R. Nickells, “BAX-depleted retinal
ganglion cells survive and become quiescent following optic nerve damage,” Molecular
Neurobiology, vol. 57, no. 2. Springer Nature, pp. 1070–1084, 2020.
ista: Donahue R, Maes ME, Grosser J, Nickells R. 2020. BAX-depleted retinal ganglion
cells survive and become quiescent following optic nerve damage. Molecular Neurobiology.
57(2), 1070–1084.
mla: Donahue, RJ, et al. “BAX-Depleted Retinal Ganglion Cells Survive and Become
Quiescent Following Optic Nerve Damage.” Molecular Neurobiology, vol. 57,
no. 2, Springer Nature, 2020, pp. 1070–1084, doi:10.1007/s12035-019-01783-7.
short: R. Donahue, M.E. Maes, J. Grosser, R. Nickells, Molecular Neurobiology 57
(2020) 1070–1084.
date_created: 2019-11-18T14:18:39Z
date_published: 2020-02-01T00:00:00Z
date_updated: 2023-08-17T14:05:48Z
day: '01'
department:
- _id: SaSi
doi: 10.1007/s12035-019-01783-7
external_id:
isi:
- '000493754200001'
pmid:
- '31673950'
fulldoi: https://doi.org/10.1007/s12035-019-01783-7
intvolume: ' 57'
isi: 1
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7035206/
month: '02'
oa: 1
oa_version: Submitted Version
page: 1070–1084
pmid: 1
publication: Molecular Neurobiology
publication_identifier:
eissn:
- 1559-1182
issn:
- 0893-7648
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: BAX-depleted retinal ganglion cells survive and become quiescent following
optic nerve damage
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 57
year: '2020'
...
---
_id: '7369'
abstract:
- lang: eng
text: Neuronal responses to complex stimuli and tasks can encompass a wide range
of time scales. Understanding these responses requires measures that characterize
how the information on these response patterns are represented across multiple
temporal resolutions. In this paper we propose a metric – which we call multiscale
relevance (MSR) – to capture the dynamical variability of the activity of single
neurons across different time scales. The MSR is a non-parametric, fully featureless
indicator in that it uses only the time stamps of the firing activity without
resorting to any a priori covariate or invoking any specific structure in the
tuning curve for neural activity. When applied to neural data from the mEC and
from the ADn and PoS regions of freely-behaving rodents, we found that neurons
having low MSR tend to have low mutual information and low firing sparsity across
the correlates that are believed to be encoded by the region of the brain where
the recordings were made. In addition, neurons with high MSR contain significant
information on spatial navigation and allow to decode spatial position or head
direction as efficiently as those neurons whose firing activity has high mutual
information with the covariate to be decoded and significantly better than the
set of neurons with high local variations in their interspike intervals. Given
these results, we propose that the MSR can be used as a measure to rank and select
neurons for their information content without the need to appeal to any a priori
covariate.
acknowledgement: This research was supported by the Kavli Foundation and the Centre
of Excellence scheme of the Research Council of Norway (Centre for Neural Computation).
RJC is currently receiving funding from the European Union’s Horizon 2020 research
and innovation programme under the Marie Skłodowska-Curie Grant Agreement No. 754411.
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Ryan J
full_name: Cubero, Ryan J
id: 850B2E12-9CD4-11E9-837F-E719E6697425
last_name: Cubero
orcid: 0000-0003-0002-1867
- first_name: Matteo
full_name: Marsili, Matteo
last_name: Marsili
- first_name: Yasser
full_name: Roudi, Yasser
last_name: Roudi
citation:
ama: Cubero RJ, Marsili M, Roudi Y. Multiscale relevance and informative encoding
in neuronal spike trains. Journal of Computational Neuroscience. 2020;48:85-102.
doi:10.1007/s10827-020-00740-x
apa: Cubero, R. J., Marsili, M., & Roudi, Y. (2020). Multiscale relevance and
informative encoding in neuronal spike trains. Journal of Computational Neuroscience.
Springer Nature. https://doi.org/10.1007/s10827-020-00740-x
chicago: Cubero, Ryan J, Matteo Marsili, and Yasser Roudi. “Multiscale Relevance
and Informative Encoding in Neuronal Spike Trains.” Journal of Computational
Neuroscience. Springer Nature, 2020. https://doi.org/10.1007/s10827-020-00740-x.
ieee: R. J. Cubero, M. Marsili, and Y. Roudi, “Multiscale relevance and informative
encoding in neuronal spike trains,” Journal of Computational Neuroscience,
vol. 48. Springer Nature, pp. 85–102, 2020.
ista: Cubero RJ, Marsili M, Roudi Y. 2020. Multiscale relevance and informative
encoding in neuronal spike trains. Journal of Computational Neuroscience. 48,
85–102.
mla: Cubero, Ryan J., et al. “Multiscale Relevance and Informative Encoding in Neuronal
Spike Trains.” Journal of Computational Neuroscience, vol. 48, Springer
Nature, 2020, pp. 85–102, doi:10.1007/s10827-020-00740-x.
short: R.J. Cubero, M. Marsili, Y. Roudi, Journal of Computational Neuroscience
48 (2020) 85–102.
corr_author: '1'
date_created: 2020-01-28T10:34:00Z
date_published: 2020-02-01T00:00:00Z
date_updated: 2025-04-14T07:44:02Z
day: '01'
ddc:
- '004'
- '519'
- '570'
department:
- _id: SaSi
doi: 10.1007/s10827-020-00740-x
ec_funded: 1
external_id:
isi:
- '000515321800006'
file:
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checksum: 036e9451d6cd0c190ad25791bf82393b
content_type: application/pdf
creator: rcubero
date_created: 2020-01-28T09:31:09Z
date_updated: 2020-07-14T12:47:56Z
file_id: '7380'
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file_size: 1941355
relation: supplementary_material
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checksum: 4dd8b1fd4b54486f79d82ac7b2a412b2
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creator: rcubero
date_created: 2020-01-28T09:31:09Z
date_updated: 2020-07-14T12:47:56Z
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file_size: 3257880
relation: main_file
file_date_updated: 2020-07-14T12:47:56Z
fulldoi: https://doi.org/10.1007/s10827-020-00740-x
has_accepted_license: '1'
intvolume: ' 48'
isi: 1
keyword:
- Time series analysis
- Multiple time scale analysis
- Spike train data
- Information theory
- Bayesian decoding
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 85-102
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
publication: Journal of Computational Neuroscience
publication_identifier:
eissn:
- 1573-6873
issn:
- 0929-5313
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Multiscale relevance and informative encoding in neuronal spike trains
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 48
year: '2020'
...
---
_id: '6412'
abstract:
- lang: eng
text: Polycomb group (PcG) proteins play critical roles in the epigenetic inheritance
of cell fate. The Polycomb Repressive Complexes PRC1 and PRC2 catalyse distinct
chromatin modifications to enforce gene silencing, but how transcriptional repression
is propagated through mitotic cell divisions remains a key unresolved question.
Using reversible tethering of PcG proteins to ectopic sites in mouse embryonic
stem cells, here we show that PRC1 can trigger transcriptional repression and
Polycomb-dependent chromatin modifications. We find that canonical PRC1 (cPRC1),
but not variant PRC1, maintains gene silencing through cell division upon reversal
of tethering. Propagation of gene repression is sustained by cis-acting histone
modifications, PRC2-mediated H3K27me3 and cPRC1-mediated H2AK119ub1, promoting
a sequence-independent feedback mechanism for PcG protein recruitment. Thus, the
distinct PRC1 complexes present in vertebrates can differentially regulate epigenetic
maintenance of gene silencing, potentially enabling dynamic heritable responses
to complex stimuli. Our findings reveal how PcG repression is potentially inherited
in vertebrates.
article_number: '1931'
article_processing_charge: No
author:
- first_name: Hagar F.
full_name: Moussa, Hagar F.
last_name: Moussa
- first_name: Daniel
full_name: Bsteh, Daniel
last_name: Bsteh
- first_name: Ramesh
full_name: Yelagandula, Ramesh
last_name: Yelagandula
- first_name: Carina
full_name: Pribitzer, Carina
last_name: Pribitzer
- first_name: Karin
full_name: Stecher, Karin
last_name: Stecher
- first_name: Katarina
full_name: Bartalska, Katarina
id: 4D883232-F248-11E8-B48F-1D18A9856A87
last_name: Bartalska
- first_name: Luca
full_name: Michetti, Luca
last_name: Michetti
- first_name: Jingkui
full_name: Wang, Jingkui
last_name: Wang
- first_name: Jorge A.
full_name: Zepeda-Martinez, Jorge A.
last_name: Zepeda-Martinez
- first_name: Ulrich
full_name: Elling, Ulrich
last_name: Elling
- first_name: Jacob I.
full_name: Stuckey, Jacob I.
last_name: Stuckey
- first_name: Lindsey I.
full_name: James, Lindsey I.
last_name: James
- first_name: Stephen V.
full_name: Frye, Stephen V.
last_name: Frye
- first_name: Oliver
full_name: Bell, Oliver
last_name: Bell
citation:
ama: Moussa HF, Bsteh D, Yelagandula R, et al. Canonical PRC1 controls sequence-independent
propagation of Polycomb-mediated gene silencing. Nature Communications.
2019;10(1). doi:10.1038/s41467-019-09628-6
apa: Moussa, H. F., Bsteh, D., Yelagandula, R., Pribitzer, C., Stecher, K., Bartalska,
K., … Bell, O. (2019). Canonical PRC1 controls sequence-independent propagation
of Polycomb-mediated gene silencing. Nature Communications. Springer Nature.
https://doi.org/10.1038/s41467-019-09628-6
chicago: Moussa, Hagar F., Daniel Bsteh, Ramesh Yelagandula, Carina Pribitzer, Karin
Stecher, Katarina Bartalska, Luca Michetti, et al. “Canonical PRC1 Controls Sequence-Independent
Propagation of Polycomb-Mediated Gene Silencing.” Nature Communications.
Springer Nature, 2019. https://doi.org/10.1038/s41467-019-09628-6.
ieee: H. F. Moussa et al., “Canonical PRC1 controls sequence-independent
propagation of Polycomb-mediated gene silencing,” Nature Communications,
vol. 10, no. 1. Springer Nature, 2019.
ista: Moussa HF, Bsteh D, Yelagandula R, Pribitzer C, Stecher K, Bartalska K, Michetti
L, Wang J, Zepeda-Martinez JA, Elling U, Stuckey JI, James LI, Frye SV, Bell O.
2019. Canonical PRC1 controls sequence-independent propagation of Polycomb-mediated
gene silencing. Nature Communications. 10(1), 1931.
mla: Moussa, Hagar F., et al. “Canonical PRC1 Controls Sequence-Independent Propagation
of Polycomb-Mediated Gene Silencing.” Nature Communications, vol. 10, no.
1, 1931, Springer Nature, 2019, doi:10.1038/s41467-019-09628-6.
short: H.F. Moussa, D. Bsteh, R. Yelagandula, C. Pribitzer, K. Stecher, K. Bartalska,
L. Michetti, J. Wang, J.A. Zepeda-Martinez, U. Elling, J.I. Stuckey, L.I. James,
S.V. Frye, O. Bell, Nature Communications 10 (2019).
date_created: 2019-05-13T07:58:35Z
date_published: 2019-04-29T00:00:00Z
date_updated: 2026-04-03T09:38:23Z
day: '29'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1038/s41467-019-09628-6
external_id:
isi:
- '000466118700002'
file:
- access_level: open_access
checksum: 6550a328335396c856db4cbdda7d2994
content_type: application/pdf
creator: dernst
date_created: 2019-05-14T08:45:51Z
date_updated: 2020-07-14T12:47:29Z
file_id: '6448'
file_name: 2019_NatureComm_Moussa.pdf
file_size: 1223647
relation: main_file
file_date_updated: 2020-07-14T12:47:29Z
fulldoi: https://doi.org/10.1038/s41467-019-09628-6
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
issue: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Canonical PRC1 controls sequence-independent propagation of Polycomb-mediated
gene silencing
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 10
year: '2019'
...
---
_id: '6521'
abstract:
- lang: eng
text: Microglia have emerged as a critical component of neurodegenerative diseases.
Genetic manipulation of microglia can elucidate their functional impact in disease.
In neuroscience, recombinant viruses such as lentiviruses and adeno-associated
viruses (AAVs) have been successfully used to target various cell types in the
brain, although effective transduction of microglia is rare. In this review, we
provide a short background of lentiviruses and AAVs, and strategies for designing
recombinant viral vectors. Then, we will summarize recent literature on successful
microglial transductions in vitro and in vivo, and discuss the current challenges.
Finally, we provide guidelines for reporting the efficiency and specificity of
viral targeting in microglia, which will enable the microglial research community
to assess and improve methodologies for future studies.
article_number: '134310'
article_processing_charge: No
article_type: original
author:
- first_name: Margaret E
full_name: Maes, Margaret E
id: 3838F452-F248-11E8-B48F-1D18A9856A87
last_name: Maes
orcid: 0000-0001-9642-1085
- first_name: Gloria
full_name: Colombo, Gloria
id: 3483CF6C-F248-11E8-B48F-1D18A9856A87
last_name: Colombo
orcid: 0000-0001-9434-8902
- first_name: Rouven
full_name: Schulz, Rouven
id: 4C5E7B96-F248-11E8-B48F-1D18A9856A87
last_name: Schulz
orcid: 0000-0001-5297-733X
- first_name: Sandra
full_name: Siegert, Sandra
id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
last_name: Siegert
orcid: 0000-0001-8635-0877
citation:
ama: 'Maes ME, Colombo G, Schulz R, Siegert S. Targeting microglia with lentivirus
and AAV: Recent advances and remaining challenges. Neuroscience Letters.
2019;707. doi:10.1016/j.neulet.2019.134310'
apa: 'Maes, M. E., Colombo, G., Schulz, R., & Siegert, S. (2019). Targeting
microglia with lentivirus and AAV: Recent advances and remaining challenges. Neuroscience
Letters. Elsevier. https://doi.org/10.1016/j.neulet.2019.134310'
chicago: 'Maes, Margaret E, Gloria Colombo, Rouven Schulz, and Sandra Siegert. “Targeting
Microglia with Lentivirus and AAV: Recent Advances and Remaining Challenges.”
Neuroscience Letters. Elsevier, 2019. https://doi.org/10.1016/j.neulet.2019.134310.'
ieee: 'M. E. Maes, G. Colombo, R. Schulz, and S. Siegert, “Targeting microglia with
lentivirus and AAV: Recent advances and remaining challenges,” Neuroscience
Letters, vol. 707. Elsevier, 2019.'
ista: 'Maes ME, Colombo G, Schulz R, Siegert S. 2019. Targeting microglia with lentivirus
and AAV: Recent advances and remaining challenges. Neuroscience Letters. 707,
134310.'
mla: 'Maes, Margaret E., et al. “Targeting Microglia with Lentivirus and AAV: Recent
Advances and Remaining Challenges.” Neuroscience Letters, vol. 707, 134310,
Elsevier, 2019, doi:10.1016/j.neulet.2019.134310.'
short: M.E. Maes, G. Colombo, R. Schulz, S. Siegert, Neuroscience Letters 707 (2019).
corr_author: '1'
date_created: 2019-06-05T13:16:24Z
date_published: 2019-08-10T00:00:00Z
date_updated: 2025-03-31T16:01:17Z
day: '10'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1016/j.neulet.2019.134310
ec_funded: 1
external_id:
isi:
- '000486094600037'
pmid:
- '31158432'
file:
- access_level: open_access
checksum: 553c9dbd39727fbed55ee991c51ca4d1
content_type: application/pdf
creator: dernst
date_created: 2019-06-08T11:44:20Z
date_updated: 2020-07-14T12:47:33Z
file_id: '6551'
file_name: 2019_Neuroscience_Maes.pdf
file_size: 1779287
relation: main_file
file_date_updated: 2020-07-14T12:47:33Z
fulldoi: https://doi.org/10.1016/j.neulet.2019.134310
has_accepted_license: '1'
intvolume: ' 707'
isi: 1
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
- _id: 25D4A630-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '715571'
name: Microglia action towards neuronal circuit formation and function in health
and disease
- _id: 267F75D8-B435-11E9-9278-68D0E5697425
name: Modulating microglia through G protein-coupled receptor (GPCR) signaling
publication: Neuroscience Letters
publication_identifier:
issn:
- 0304-3940
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Targeting microglia with lentivirus and AAV: Recent advances and remaining
challenges'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 707
year: '2019'
...
---
_id: '7095'
abstract:
- lang: eng
text: BAX, a member of the BCL2 gene family, controls the committed step of the
intrinsic apoptotic program. Mitochondrial fragmentation is a commonly observed
feature of apoptosis, which occurs through the process of mitochondrial fission.
BAX has consistently been associated with mitochondrial fission, yet how BAX participates
in the process of mitochondrial fragmentation during apoptosis remains to be tested.
Time-lapse imaging of BAX recruitment and mitochondrial fragmentation demonstrates
that rapid mitochondrial fragmentation during apoptosis occurs after the complete
recruitment of BAX to the mitochondrial outer membrane (MOM). The requirement
of a fully functioning BAX protein for the fission process was demonstrated further
in BAX/BAK-deficient HCT116 cells expressing a P168A mutant of BAX. The mutant
performed fusion to restore the mitochondrial network. but was not demonstrably
recruited to the MOM after apoptosis induction. Under these conditions, mitochondrial
fragmentation was blocked. Additionally, we show that loss of the fission protein,
dynamin-like protein 1 (DRP1), does not temporally affect the initiation time
or rate of BAX recruitment, but does reduce the final level of BAX recruited to
the MOM during the late phase of BAX recruitment. These correlative observations
suggest a model where late-stage BAX oligomers play a functional part of the mitochondrial
fragmentation machinery in apoptotic cells.
article_number: '16565'
article_processing_charge: No
article_type: original
author:
- first_name: Margaret E
full_name: Maes, Margaret E
id: 3838F452-F248-11E8-B48F-1D18A9856A87
last_name: Maes
orcid: 0000-0001-9642-1085
- first_name: J. A.
full_name: Grosser, J. A.
last_name: Grosser
- first_name: R. L.
full_name: Fehrman, R. L.
last_name: Fehrman
- first_name: C. L.
full_name: Schlamp, C. L.
last_name: Schlamp
- first_name: R. W.
full_name: Nickells, R. W.
last_name: Nickells
citation:
ama: Maes ME, Grosser JA, Fehrman RL, Schlamp CL, Nickells RW. Completion of BAX
recruitment correlates with mitochondrial fission during apoptosis. Scientific
Reports. 2019;9. doi:10.1038/s41598-019-53049-w
apa: Maes, M. E., Grosser, J. A., Fehrman, R. L., Schlamp, C. L., & Nickells,
R. W. (2019). Completion of BAX recruitment correlates with mitochondrial fission
during apoptosis. Scientific Reports. Springer Nature. https://doi.org/10.1038/s41598-019-53049-w
chicago: Maes, Margaret E, J. A. Grosser, R. L. Fehrman, C. L. Schlamp, and R. W.
Nickells. “Completion of BAX Recruitment Correlates with Mitochondrial Fission
during Apoptosis.” Scientific Reports. Springer Nature, 2019. https://doi.org/10.1038/s41598-019-53049-w.
ieee: M. E. Maes, J. A. Grosser, R. L. Fehrman, C. L. Schlamp, and R. W. Nickells,
“Completion of BAX recruitment correlates with mitochondrial fission during apoptosis,”
Scientific Reports, vol. 9. Springer Nature, 2019.
ista: Maes ME, Grosser JA, Fehrman RL, Schlamp CL, Nickells RW. 2019. Completion
of BAX recruitment correlates with mitochondrial fission during apoptosis. Scientific
Reports. 9, 16565.
mla: Maes, Margaret E., et al. “Completion of BAX Recruitment Correlates with Mitochondrial
Fission during Apoptosis.” Scientific Reports, vol. 9, 16565, Springer
Nature, 2019, doi:10.1038/s41598-019-53049-w.
short: M.E. Maes, J.A. Grosser, R.L. Fehrman, C.L. Schlamp, R.W. Nickells, Scientific
Reports 9 (2019).
date_created: 2019-11-25T07:45:17Z
date_published: 2019-11-12T00:00:00Z
date_updated: 2023-08-30T07:26:54Z
day: '12'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1038/s41598-019-53049-w
external_id:
isi:
- '000495857600019'
pmid:
- '31719602'
file:
- access_level: open_access
checksum: 9ab397ed9c1c454b34bffb8cc863d734
content_type: application/pdf
creator: dernst
date_created: 2019-11-25T07:49:52Z
date_updated: 2020-07-14T12:47:49Z
file_id: '7096'
file_name: 2019_ScientificReports_Maes.pdf
file_size: 6467393
relation: main_file
file_date_updated: 2020-07-14T12:47:49Z
fulldoi: https://doi.org/10.1038/s41598-019-53049-w
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: Scientific Reports
publication_identifier:
eissn:
- 2045-2322
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Completion of BAX recruitment correlates with mitochondrial fission during
apoptosis
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 9
year: '2019'
...
---
_id: '32'
abstract:
- lang: eng
text: The functional role of AMPA receptor (AMPAR)-mediated synaptic signaling between
neurons and oligodendrocyte precursor cells (OPCs) remains enigmatic. We modified
the properties of AMPARs at axon-OPC synapses in the mouse corpus callosum in
vivo during the peak of myelination by targeting the GluA2 subunit. Expression
of the unedited (Ca2+ permeable) or the pore-dead GluA2 subunit of AMPARs triggered
proliferation of OPCs and reduced their differentiation into oligodendrocytes.
Expression of the cytoplasmic C-terminal (GluA2(813-862)) of the GluA2 subunit
(C-tail), a modification designed to affect the interaction between GluA2 and
AMPAR-binding proteins and to perturb trafficking of GluA2-containing AMPARs,
decreased the differentiation of OPCs without affecting their proliferation. These
findings suggest that ionotropic and non-ionotropic properties of AMPARs in OPCs,
as well as specific aspects of AMPAR-mediated signaling at axon-OPC synapses in
the mouse corpus callosum, are important for balancing the response of OPCs to
proliferation and differentiation cues. In the brain, oligodendrocyte precursor
cells (OPCs) receive glutamatergic AMPA-receptor-mediated synaptic input from
neurons. Chen et al. show that modifying AMPA-receptor properties at axon-OPC
synapses alters proliferation and differentiation of OPCs. This expands the traditional
view of synaptic transmission by suggesting neurons also use synapses to modulate
behavior of glia.
acknowledgement: This work was supported by Deutsche Forschungsgemeinschaft (DFG)
grant KU2569/1-1 (to M.K.); DFG project EXC307Centre for Integrative Neuroscience
(CIN), including grant Pool Project 2011-12 (jointly to M.K. and I.E.); and the
Charitable Hertie Foundation (to I.E.). CIN is an Excellence Cluster funded by the
DFG within the framework of the Excellence Initiative for 2008–2018. M.K. is supported
by the Tistou & Charlotte Kerstan Foundation.
article_processing_charge: No
author:
- first_name: Ting
full_name: Chen, Ting
last_name: Chen
- first_name: Bartosz
full_name: Kula, Bartosz
last_name: Kula
- first_name: Balint
full_name: Nagy, Balint
id: 30F830CE-02D1-11E9-9BAA-DAF4881429F2
last_name: Nagy
orcid: 0000-0002-4002-4686
- first_name: Ruxandra
full_name: Barzan, Ruxandra
last_name: Barzan
- first_name: Andrea
full_name: Gall, Andrea
last_name: Gall
- first_name: Ingrid
full_name: Ehrlich, Ingrid
last_name: Ehrlich
- first_name: Maria
full_name: Kukley, Maria
last_name: Kukley
citation:
ama: Chen T, Kula B, Nagy B, et al. In Vivo regulation of Oligodendrocyte processor
cell proliferation and differentiation by the AMPA-receptor Subunit GluA2. Cell
Reports. 2018;25(4):852-861.e7. doi:10.1016/j.celrep.2018.09.066
apa: Chen, T., Kula, B., Nagy, B., Barzan, R., Gall, A., Ehrlich, I., & Kukley,
M. (2018). In Vivo regulation of Oligodendrocyte processor cell proliferation
and differentiation by the AMPA-receptor Subunit GluA2. Cell Reports. Elsevier.
https://doi.org/10.1016/j.celrep.2018.09.066
chicago: Chen, Ting, Bartosz Kula, Balint Nagy, Ruxandra Barzan, Andrea Gall, Ingrid
Ehrlich, and Maria Kukley. “In Vivo Regulation of Oligodendrocyte Processor Cell
Proliferation and Differentiation by the AMPA-Receptor Subunit GluA2.” Cell
Reports. Elsevier, 2018. https://doi.org/10.1016/j.celrep.2018.09.066.
ieee: T. Chen et al., “In Vivo regulation of Oligodendrocyte processor cell
proliferation and differentiation by the AMPA-receptor Subunit GluA2,” Cell
Reports, vol. 25, no. 4. Elsevier, p. 852–861.e7, 2018.
ista: Chen T, Kula B, Nagy B, Barzan R, Gall A, Ehrlich I, Kukley M. 2018. In Vivo
regulation of Oligodendrocyte processor cell proliferation and differentiation
by the AMPA-receptor Subunit GluA2. Cell Reports. 25(4), 852–861.e7.
mla: Chen, Ting, et al. “In Vivo Regulation of Oligodendrocyte Processor Cell Proliferation
and Differentiation by the AMPA-Receptor Subunit GluA2.” Cell Reports,
vol. 25, no. 4, Elsevier, 2018, p. 852–861.e7, doi:10.1016/j.celrep.2018.09.066.
short: T. Chen, B. Kula, B. Nagy, R. Barzan, A. Gall, I. Ehrlich, M. Kukley, Cell
Reports 25 (2018) 852–861.e7.
date_created: 2018-12-11T11:44:16Z
date_published: 2018-10-23T00:00:00Z
date_updated: 2023-09-11T14:13:32Z
day: '23'
ddc:
- '570'
department:
- _id: SaSi
doi: 10.1016/j.celrep.2018.09.066
external_id:
isi:
- '000448219500005'
file:
- access_level: open_access
checksum: d9f74277fd57176e04732707d575cf08
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T12:42:57Z
date_updated: 2020-07-14T12:46:03Z
file_id: '5703'
file_name: 2018_CellReports_Chen.pdf
file_size: 4461997
relation: main_file
file_date_updated: 2020-07-14T12:46:03Z
fulldoi: https://doi.org/10.1016/j.celrep.2018.09.066
has_accepted_license: '1'
intvolume: ' 25'
isi: 1
issue: '4'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: 852 - 861.e7
publication: Cell Reports
publication_status: published
publisher: Elsevier
publist_id: '8023'
quality_controlled: '1'
scopus_import: '1'
status: public
title: In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation
by the AMPA-receptor Subunit GluA2
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 25
year: '2018'
...
---
_id: '708'
abstract:
- lang: eng
text: 'In the developing and adult brain, oligodendrocyte precursor cells (OPCs)
are influenced by neuronal activity: they are involved in synaptic signaling with
neurons, and their proliferation and differentiation into myelinating glia can
be altered by transient changes in neuronal firing. An important question that
has been unanswered is whether OPCs can discriminate different patterns of neuronal
activity and respond to them in a distinct way. Here, we demonstrate in brain
slices that the pattern of neuronal activity determines the functional changes
triggered at synapses between axons and OPCs. Furthermore, we show that stimulation
of the corpus callosum at different frequencies in vivo affects proliferation
and differentiation of OPCs in a dissimilar way. Our findings suggest that neurons
do not influence OPCs in “all-or-none” fashion but use their firing pattern to
tune the response and behavior of these nonneuronal cells.'
article_number: e2001993
article_processing_charge: No
author:
- first_name: Balint
full_name: Nagy, Balint
id: 30F830CE-02D1-11E9-9BAA-DAF4881429F2
last_name: Nagy
orcid: 0000-0002-4002-4686
- first_name: Anahit
full_name: Hovhannisyan, Anahit
last_name: Hovhannisyan
- first_name: Ruxandra
full_name: Barzan, Ruxandra
last_name: Barzan
- first_name: Ting
full_name: Chen, Ting
last_name: Chen
- first_name: Maria
full_name: Kukley, Maria
last_name: Kukley
citation:
ama: Nagy B, Hovhannisyan A, Barzan R, Chen T, Kukley M. Different patterns of neuronal
activity trigger distinct responses of oligodendrocyte precursor cells in the
corpus callosum. PLoS Biology. 2017;15(8). doi:10.1371/journal.pbio.2001993
apa: Nagy, B., Hovhannisyan, A., Barzan, R., Chen, T., & Kukley, M. (2017).
Different patterns of neuronal activity trigger distinct responses of oligodendrocyte
precursor cells in the corpus callosum. PLoS Biology. Public Library of
Science. https://doi.org/10.1371/journal.pbio.2001993
chicago: Nagy, Balint, Anahit Hovhannisyan, Ruxandra Barzan, Ting Chen, and Maria
Kukley. “Different Patterns of Neuronal Activity Trigger Distinct Responses of
Oligodendrocyte Precursor Cells in the Corpus Callosum.” PLoS Biology.
Public Library of Science, 2017. https://doi.org/10.1371/journal.pbio.2001993.
ieee: B. Nagy, A. Hovhannisyan, R. Barzan, T. Chen, and M. Kukley, “Different patterns
of neuronal activity trigger distinct responses of oligodendrocyte precursor cells
in the corpus callosum,” PLoS Biology, vol. 15, no. 8. Public Library of
Science, 2017.
ista: Nagy B, Hovhannisyan A, Barzan R, Chen T, Kukley M. 2017. Different patterns
of neuronal activity trigger distinct responses of oligodendrocyte precursor cells
in the corpus callosum. PLoS Biology. 15(8), e2001993.
mla: Nagy, Balint, et al. “Different Patterns of Neuronal Activity Trigger Distinct
Responses of Oligodendrocyte Precursor Cells in the Corpus Callosum.” PLoS
Biology, vol. 15, no. 8, e2001993, Public Library of Science, 2017, doi:10.1371/journal.pbio.2001993.
short: B. Nagy, A. Hovhannisyan, R. Barzan, T. Chen, M. Kukley, PLoS Biology 15
(2017).
corr_author: '1'
date_created: 2018-12-11T11:48:03Z
date_published: 2017-08-22T00:00:00Z
date_updated: 2025-09-10T11:05:19Z
day: '22'
ddc:
- '576'
- '610'
department:
- _id: SaSi
doi: 10.1371/journal.pbio.2001993
external_id:
isi:
- '000408756200005'
file:
- access_level: open_access
checksum: 0c974f430682dc832ea7b27ab5a93124
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:35Z
date_updated: 2020-07-14T12:47:49Z
file_id: '5156'
file_name: IST-2017-889-v1+1_journal.pbio.2001993.pdf
file_size: 18155365
relation: main_file
file_date_updated: 2020-07-14T12:47:49Z
fulldoi: https://doi.org/10.1371/journal.pbio.2001993
has_accepted_license: '1'
intvolume: ' 15'
isi: 1
issue: '8'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
publication: PLoS Biology
publication_identifier:
issn:
- 1544-9173
publication_status: published
publisher: Public Library of Science
publist_id: '6983'
pubrep_id: '889'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Different patterns of neuronal activity trigger distinct responses of oligodendrocyte
precursor cells in the corpus callosum
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 15
year: '2017'
...
---
_id: '557'
abstract:
- lang: eng
text: PURPOSE. Gene therapy of retinal ganglion cells (RGCs) has promise as a powerful
therapeutic for the rescue and regeneration of these cells after optic nerve damage.
However, early after damage, RGCs undergo atrophic changes, including gene silencing.
It is not known if these changes will deleteriously affect transduction and transgene
expression, or if the therapeutic protein can influence reactivation of the endogenous
genome. METHODS. Double-transgenic mice carrying a Rosa26-(LoxP)-tdTomato reporter,
and a mutant allele for the proapoptotic Bax gene were reared. The Bax mutant
blocks apoptosis, but RGCs still exhibit nuclear atrophy and gene silencing. At
times ranging from 1 hour to 4 weeks after optic nerve crush (ONC), eyes received
an intravitreal injection of AAV2 virus carrying the Cre recombinase. Successful
transduction was monitored by expression of the tdTomato reporter. Immunostaining
was used to localize tdTomato expression in select cell types. RESULTS. Successful
transduction of RGCs was achieved at all time points after ONC using AAV2 expressing
Cre from the phosphoglycerate kinase (Pgk) promoter, but not the CMV promoter.
ONC promoted an increase in the transduction of cell types in the inner nuclear
layer, including Müller cells and rod bipolar neurons. There was minimal evidence
of transduction of amacrine cells and astrocytes in the inner retina or optic
nerve. CONCLUSIONS. Damaged RGCs can be transduced and at least some endogenous
genes can be subsequently activated. Optic nerve damage may change retinal architecture
to allow greater penetration of an AAV2 virus to transduce several additional
cell types in the inner nuclear layer.
article_processing_charge: No
author:
- first_name: Robert
full_name: Nickells, Robert
last_name: Nickells
- first_name: Heather
full_name: Schmitt, Heather
last_name: Schmitt
- first_name: Margaret E
full_name: Maes, Margaret E
id: 3838F452-F248-11E8-B48F-1D18A9856A87
last_name: Maes
orcid: 0000-0001-9642-1085
- first_name: Cassandra
full_name: Schlamp, Cassandra
last_name: Schlamp
citation:
ama: Nickells R, Schmitt H, Maes ME, Schlamp C. AAV2 mediated transduction of the
mouse retina after optic nerve injury. Investigative Ophthalmology and Visual
Science. 2017;58(14):6091-6104. doi:10.1167/iovs.17-22634
apa: Nickells, R., Schmitt, H., Maes, M. E., & Schlamp, C. (2017). AAV2 mediated
transduction of the mouse retina after optic nerve injury. Investigative Ophthalmology
and Visual Science. Association for Research in Vision & Ophthalmology.
https://doi.org/10.1167/iovs.17-22634
chicago: Nickells, Robert, Heather Schmitt, Margaret E Maes, and Cassandra Schlamp.
“AAV2 Mediated Transduction of the Mouse Retina after Optic Nerve Injury.” Investigative
Ophthalmology and Visual Science. Association for Research in Vision &
Ophthalmology, 2017. https://doi.org/10.1167/iovs.17-22634.
ieee: R. Nickells, H. Schmitt, M. E. Maes, and C. Schlamp, “AAV2 mediated transduction
of the mouse retina after optic nerve injury,” Investigative Ophthalmology
and Visual Science, vol. 58, no. 14. Association for Research in Vision &
Ophthalmology, pp. 6091–6104, 2017.
ista: Nickells R, Schmitt H, Maes ME, Schlamp C. 2017. AAV2 mediated transduction
of the mouse retina after optic nerve injury. Investigative Ophthalmology and
Visual Science. 58(14), 6091–6104.
mla: Nickells, Robert, et al. “AAV2 Mediated Transduction of the Mouse Retina after
Optic Nerve Injury.” Investigative Ophthalmology and Visual Science, vol.
58, no. 14, Association for Research in Vision & Ophthalmology, 2017, pp.
6091–104, doi:10.1167/iovs.17-22634.
short: R. Nickells, H. Schmitt, M.E. Maes, C. Schlamp, Investigative Ophthalmology
and Visual Science 58 (2017) 6091–6104.
date_created: 2018-12-11T11:47:10Z
date_published: 2017-12-14T00:00:00Z
date_updated: 2026-08-12T11:16:45Z
day: '14'
ddc:
- '576'
department:
- _id: SaSi
doi: 10.1167/iovs.17-22634
external_id:
isi:
- '000426781300012'
file:
- access_level: open_access
checksum: d7a7b6f1fa9211a04e5e65634a0265d9
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:53Z
date_updated: 2020-07-14T12:47:04Z
file_id: '5311'
file_name: IST-2018-920-v1+1_i1552-5783-58-14-6091.pdf
file_size: 2955559
relation: main_file
file_date_updated: 2020-07-14T12:47:04Z
fulldoi: https://doi.org/10.1167/iovs.17-22634
has_accepted_license: '1'
intvolume: ' 58'
isi: 1
issue: '14'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 6091 - 6104
publication: Investigative Ophthalmology and Visual Science
publication_identifier:
issn:
- 0146-0404
publication_status: published
publisher: Association for Research in Vision & Ophthalmology
publist_id: '7254'
pubrep_id: '920'
quality_controlled: '1'
scopus_import: '1'
status: public
title: AAV2 mediated transduction of the mouse retina after optic nerve injury
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 58
year: '2017'
...
---
_id: '1253'
abstract:
- lang: eng
text: This article provides an introduction to the role of microRNAs in the nervous
system and outlines their potential involvement in the pathophysiology of schizophrenia,
which is hypothesized to arise owing to environmental factors and genetic predisposition.
article_processing_charge: No
author:
- first_name: Lihuei
full_name: Tsai, Lihuei
last_name: Tsai
- first_name: Sandra
full_name: Siegert, Sandra
id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
last_name: Siegert
orcid: 0000-0001-8635-0877
citation:
ama: Tsai L, Siegert S. How MicroRNAs Are involved in splitting the mind. JAMA
Psychiatry. 2016;73(4):409-410. doi:10.1001/jamapsychiatry.2015.3144
apa: Tsai, L., & Siegert, S. (2016). How MicroRNAs Are involved in splitting
the mind. JAMA Psychiatry. American Medical Association. https://doi.org/10.1001/jamapsychiatry.2015.3144
chicago: Tsai, Lihuei, and Sandra Siegert. “How MicroRNAs Are Involved in Splitting
the Mind.” JAMA Psychiatry. American Medical Association, 2016. https://doi.org/10.1001/jamapsychiatry.2015.3144.
ieee: L. Tsai and S. Siegert, “How MicroRNAs Are involved in splitting the mind,”
JAMA Psychiatry, vol. 73, no. 4. American Medical Association, pp. 409–410,
2016.
ista: Tsai L, Siegert S. 2016. How MicroRNAs Are involved in splitting the mind.
JAMA Psychiatry. 73(4), 409–410.
mla: Tsai, Lihuei, and Sandra Siegert. “How MicroRNAs Are Involved in Splitting
the Mind.” JAMA Psychiatry, vol. 73, no. 4, American Medical Association,
2016, pp. 409–10, doi:10.1001/jamapsychiatry.2015.3144.
short: L. Tsai, S. Siegert, JAMA Psychiatry 73 (2016) 409–410.
date_created: 2018-12-11T11:50:58Z
date_published: 2016-04-01T00:00:00Z
date_updated: 2025-09-22T09:08:34Z
day: '01'
ddc:
- '576'
- '610'
department:
- _id: SaSi
doi: 10.1001/jamapsychiatry.2015.3144
external_id:
isi:
- '000373444700017'
pmid:
- '26963490'
file:
- access_level: open_access
checksum: 649aee381f30f7ef7e9efa912d41c2e3
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:24Z
date_updated: 2020-07-14T12:44:41Z
file_id: '5278'
file_name: IST-2018-981-v1+1_YNP150011_annotatedproof_FINAL.pdf
file_size: 601679
relation: main_file
file_date_updated: 2020-07-14T12:44:41Z
fulldoi: https://doi.org/10.1001/jamapsychiatry.2015.3144
has_accepted_license: '1'
intvolume: ' 73'
isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Submitted Version
page: 409 - 410
pmid: 1
publication: JAMA Psychiatry
publication_identifier:
issn:
- 2168-622X
publication_status: published
publisher: American Medical Association
publist_id: '6074'
pubrep_id: '981'
quality_controlled: '1'
scopus_import: '1'
status: public
title: How MicroRNAs Are involved in splitting the mind
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 73
year: '2016'
...