| Literature DB >> 24523410 |
Jack Jiagang Zhao1, Hong Ouyang, Jing Luo, Sherrina Patel, Yuanchao Xue, John Quach, Nicole Sfeir, Meixia Zhang, Xiangdong Fu, Sheng Ding, Shaochen Chen, Kang Zhang.
Abstract
Vision impairment caused by loss of retinal neurons affects millions of people worldwide, and currently, there is no effective treatment. Müller glia of mammalian retina may represent an under-recognized and potential source for regeneration of a wide range of retinal cell types, including retinal ganglion cells and photoreceptors. Here, we demonstrated that mouse Müller glia cells have the capacity to be reprogrammed into the retinal neuronal cell fate and are competent to give rise to photoreceptors under a defined culture condition. Inactivation of p53 released proliferation restriction of Müller glia and significantly enhanced the induction of retinal progenitor from Müller glia in culture. Moreover, following the ocular transplantation, the Müller glia-derived progenitors were differentiated toward the fates of photoreceptors and retinal ganglion cells. Together, these results demonstrate the feasibility of using Müller glia as a potential source for retinal repair and regeneration.Entities:
Keywords: Muller Glia; Muller Glia, Progenitor; Photoreceptors; Proliferation; Regeneration; Reprogramming; Retina; p53
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Year: 2014 PMID: 24523410 PMCID: PMC4002101 DOI: 10.1074/jbc.M113.532671
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157