Loss of Arid1a Promotes Neuronal Survival Following Optic Nerve Injury

Frontiers in Cellular Neuroscience
Xue-Qi PengChang-Mei Liu

Abstract

Trauma or neurodegenerative diseases trigger the retrograde death of retinal ganglion cells (RGCs), causing an irreversible functional loss. AT-rich interaction domain 1A (ARID1A), a subunit of the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complex, has been shown to play crucial roles in cell homeostasis and tissue regeneration. However, its function in adult RGC regeneration remains elusive. Here, we show that optic nerve injury induces dynamic changes of Arid1a expression. Importantly, deleting Arid1a in mice dramatically promotes RGC survival, but insignificantly impacts axon regeneration after optic nerve injury. Next, joint profiling of transcripts and accessible chromatin in mature RGCs reveals that Arid1a regulates several genes involved in apoptosis and JAK/STAT signaling pathway. Thus, our findings suggest modulation of Arid1a as a potential therapeutic strategy to promote RGC neuroprotection after damage.

References

Feb 18, 2004·Nature Reviews. Cancer·Charles W M Roberts, Stuart H Orkin
Feb 20, 2004·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Dietmar FischerLarry I Benowitz
Mar 22, 2006·Proceedings of the National Academy of Sciences of the United States of America·L E BarrettJ H Eberwine
Oct 10, 2009·Science·Darcie L MooreJeffrey L Goldberg
Dec 17, 2009·Neuron·Patrice D SmithZhigang He
Sep 29, 2011·Frontiers in Microbiology·Geoffrey L RogersRoland W Herzog
Mar 6, 2012·Nature Methods·Ben Langmead, Steven L Salzberg
Mar 30, 2012·Omics : a Journal of Integrative Biology·Guangchuang YuQing-Yu He
May 23, 2012·Proceedings of the National Academy of Sciences of the United States of America·Silmara de LimaLarry Benowitz
Sep 7, 2012·The Journal of Biological Chemistry·Ghia EuskirchenMichael Snyder
Oct 13, 2012·Nature Protocols·Ali ErtürkHans-Ulrich Dodt
Nov 7, 2012·Molecular and Cellular Biology·Ronald L ChandlerTerry Magnuson
Dec 5, 2012·International Review of Neurobiology·Xueting Luo, Kevin K Park
Apr 4, 2014·Bioinformatics·Anthony M BolgerBjoern Usadel
May 7, 2014·Nucleic Acids Research·Fidel RamírezThomas Manke
Dec 18, 2014·Genome Biology·Michael I LoveSimon Anders
Apr 22, 2015·Annual Review of Neuroscience·Joshua R Sanes, Richard H Masland
Nov 18, 2015·Oncology Reports·Takashi TakedaDaisuke Aoki
Jan 10, 2016·Experimental Neurology·Larry I BenowitzJeffrey L Goldberg
Feb 24, 2016·Neuron·Vijayendran ChandranDaniel H Geschwind
May 7, 2016·Neuron·Zhigang He, Yishi Jin
Jun 4, 2016·Histology and Histopathology·Carla Andreia AbreuAna Maria Blanco Martinez
Jul 12, 2016·Nature Neuroscience·Jung-Hwan A LimAndrew D Huberman
Nov 1, 2016·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Michael C Crair, Carol A Mason
Mar 7, 2017·Nature Methods·Rob PatroCarl Kingsford
Mar 23, 2017·Investigative Ophthalmology & Visual Science·Benjamin J YungherKevin K Park
Apr 21, 2017·Neuron·Yi-Lan WengGuo-Li Ming
Apr 27, 2017·Experimental Neurology·Nicole S StiversDavid P Stirling
Jun 10, 2017·Science·Bireswar LahaAndrew D Huberman
Sep 6, 2017·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Akintomide AparaJeffrey L Goldberg
Sep 6, 2018·Cell Reports·Xue-Wei WangFeng-Quan Zhou
Oct 3, 2018·Neural Plasticity·Camila Oliveira GoulartAna Maria Blanco Martinez
Feb 28, 2019·Genome Biology·Zhijian LiIvan G Costa

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Datasets Mentioned

BETA
GSE147844

Methods Mentioned

BETA
PCR
RNA-seq
FACS
footprinting

Software Mentioned

GENCODE
Salmon
Diffbind
Bowtie 2
TRRUST
HINT
ImageJ
GSEA
GraphPad Prism
tximport

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