Frontiers in Cellular Neuroscience (May 2020)
Loss of Arid1a Promotes Neuronal Survival Following Optic Nerve Injury
- Xue-Qi Peng,
- Xue-Qi Peng,
- Xue-Qi Peng,
- Shang-Kun Dai,
- Shang-Kun Dai,
- Shang-Kun Dai,
- Chang-Ping Li,
- Chang-Ping Li,
- Chang-Ping Li,
- Pei-Pei Liu,
- Pei-Pei Liu,
- Zhi-Meng Wang,
- Zhi-Meng Wang,
- Zhi-Meng Wang,
- Hong-Zhen Du,
- Hong-Zhen Du,
- Zhao-Qian Teng,
- Zhao-Qian Teng,
- Zhao-Qian Teng,
- Shu-Guang Yang,
- Shu-Guang Yang,
- Chang-Mei Liu,
- Chang-Mei Liu,
- Chang-Mei Liu
Affiliations
- Xue-Qi Peng
- State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences (CAS), Beijing, China
- Xue-Qi Peng
- Savaid Medical School, University of Chinese Academy of Sciences, Beijing, China
- Xue-Qi Peng
- Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China
- Shang-Kun Dai
- State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences (CAS), Beijing, China
- Shang-Kun Dai
- Savaid Medical School, University of Chinese Academy of Sciences, Beijing, China
- Shang-Kun Dai
- Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China
- Chang-Ping Li
- State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences (CAS), Beijing, China
- Chang-Ping Li
- Savaid Medical School, University of Chinese Academy of Sciences, Beijing, China
- Chang-Ping Li
- Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China
- Pei-Pei Liu
- State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences (CAS), Beijing, China
- Pei-Pei Liu
- Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China
- Zhi-Meng Wang
- State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences (CAS), Beijing, China
- Zhi-Meng Wang
- Savaid Medical School, University of Chinese Academy of Sciences, Beijing, China
- Zhi-Meng Wang
- Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China
- Hong-Zhen Du
- State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences (CAS), Beijing, China
- Hong-Zhen Du
- Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China
- Zhao-Qian Teng
- State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences (CAS), Beijing, China
- Zhao-Qian Teng
- Savaid Medical School, University of Chinese Academy of Sciences, Beijing, China
- Zhao-Qian Teng
- Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China
- Shu-Guang Yang
- State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences (CAS), Beijing, China
- Shu-Guang Yang
- Department of Orthopedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD, United States
- Chang-Mei Liu
- State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences (CAS), Beijing, China
- Chang-Mei Liu
- Savaid Medical School, University of Chinese Academy of Sciences, Beijing, China
- Chang-Mei Liu
- Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, China
- DOI
- https://doi.org/10.3389/fncel.2020.00131
- Journal volume & issue
-
Vol. 14
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.
Keywords
