ArticleNeurochemical research2017
Apobec1 Promotes Neurotoxicity-Induced Dedifferentiation of Müller Glial Cells.
Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Tet3-mediated DNA demethylation is essential for maintaining the dedifferentiation capacity of mammalian Müller glia.Frontiers in molecular neuroscience · 2025Article
- Epigenetic mechanisms of Müller glial reprogramming mediating retinal regeneration.Frontiers in cell and developmental biology · 2023Review
- Epitranscriptome Analysis of Oxidative Stressed Retinal Epithelial Cells Depicted a Possible RNA Editing Landscape of Retinal Degeneration.Antioxidants (Basel, Switzerland) · 2022Article
- Müller Glia-Mediated Retinal Regeneration.Molecular neurobiology · 2021Review
- Cellular Signaling in Müller Glia: Progenitor Cells for Regenerative and Neuroprotective Responses in Pharmacological Models of Retinal Degeneration.Journal of ophthalmology · 2019Review
- Müller Glia to Müller Glia Extracellular Vesicle-Dependent Signaling Induces Multipotency GenesASN neuroArticle
- Genetic and epigenetic regulators of retinal Müller glial cell reprogramming.Advances in ophthalmology practice and researchReview
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinal Müller glial cells in mammals acquire stem and progenitor cell properties after neurotoxic treatment. However, the molecular mechanisms underlying proliferation and dedifferentiation of adult Müller cells in the mammalian retina were unclear. In this study, treatments with N-methyl-D-aspartate (NMDA) plus epidermal growth factor (EGF) led to the proliferation of Müller cells and expression of stem cell markers including Nanog and Nestin in the retina. The increased mRNA for Nanog and Nestin were coincident with reduced methylation of a Nanog promoter and a Nestin enhancer specific in the neural stem cells, respectively. We found that Apolipoprotein B mRNA editing catalytic subunit 1 (Apobec1) was upregulated early in the retina treated with NMDA and EGF. Moreover, overexpression of Apobec1 in primary Müller cells increased expression of Nestin and reduced methylation of the Nestin enhancer. The data suggest that neurotoxicity-induced Apobec1 may promote expression of Nestin and help cell cycle reentry of retinal Müller cells via DNA demethylation. This study provides novel insights into the molecular mechanisms underlying dedifferentiation and proliferation of Müller cells in the mammalian retina.
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Registered trials
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