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Loss of Arid1a Promotes Neuronal Survival Following Optic Nerve Injury
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...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7326083/ https://www.ncbi.nlm.nih.gov/pubmed/32670021 http://dx.doi.org/10.3389/fncel.2020.00131 |
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author | Peng, Xue-Qi Dai, Shang-Kun Li, Chang-Ping Liu, Pei-Pei Wang, Zhi-Meng Du, Hong-Zhen Teng, Zhao-Qian Yang, Shu-Guang Liu, Chang-Mei |
author_facet | Peng, Xue-Qi Dai, Shang-Kun Li, Chang-Ping Liu, Pei-Pei Wang, Zhi-Meng Du, Hong-Zhen Teng, Zhao-Qian Yang, Shu-Guang Liu, Chang-Mei |
author_sort | Peng, Xue-Qi |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7326083 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-73260832020-07-14 Loss of Arid1a Promotes Neuronal Survival Following Optic Nerve Injury Peng, Xue-Qi Dai, Shang-Kun Li, Chang-Ping Liu, Pei-Pei Wang, Zhi-Meng Du, Hong-Zhen Teng, Zhao-Qian Yang, Shu-Guang Liu, Chang-Mei Front Cell Neurosci Cellular Neuroscience 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. Frontiers Media S.A. 2020-05-15 /pmc/articles/PMC7326083/ /pubmed/32670021 http://dx.doi.org/10.3389/fncel.2020.00131 Text en Copyright © 2020 Peng, Dai, Li, Liu, Wang, Du, Teng, Yang and Liu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Cellular Neuroscience Peng, Xue-Qi Dai, Shang-Kun Li, Chang-Ping Liu, Pei-Pei Wang, Zhi-Meng Du, Hong-Zhen Teng, Zhao-Qian Yang, Shu-Guang Liu, Chang-Mei Loss of Arid1a Promotes Neuronal Survival Following Optic Nerve Injury |
title | Loss of Arid1a Promotes Neuronal Survival Following Optic Nerve Injury |
title_full | Loss of Arid1a Promotes Neuronal Survival Following Optic Nerve Injury |
title_fullStr | Loss of Arid1a Promotes Neuronal Survival Following Optic Nerve Injury |
title_full_unstemmed | Loss of Arid1a Promotes Neuronal Survival Following Optic Nerve Injury |
title_short | Loss of Arid1a Promotes Neuronal Survival Following Optic Nerve Injury |
title_sort | loss of arid1a promotes neuronal survival following optic nerve injury |
topic | Cellular Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7326083/ https://www.ncbi.nlm.nih.gov/pubmed/32670021 http://dx.doi.org/10.3389/fncel.2020.00131 |
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