Cell cycle-dependent activation of proneural transcription factor expression and reactive gliosis in rat Müller glia

Retinal Müller glia have a capacity to regenerate neurons in lower vertebrates like zebrafish, but such ability is extremely limited in mammals. In zebrafish, Müller glia proliferate after injury, which promotes their neurogenic reprogramming while inhibiting reactive gliosis. In mammals, however, h...

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Published in:Scientific reports 2023-12, Vol.13 (1), p.22712-22712, Article 22712
Main Authors: Nishino, Reiko, Nomura-Komoike, Kaori, Iida, Tomohiro, Fujieda, Hiroki
Format: Article
Language:English
Subjects:
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631/532
Animals
ASCL1 protein
Cell activation
Cell Cycle
Danio rerio
Glial fibrillary acidic protein
Gliosis
Gliosis - chemically induced
Gliosis - metabolism
Humanities and Social Sciences
Mammals
Mueller cells
multidisciplinary
N-Methyl-N-nitrosourea
Neuroglia - metabolism
Neuronal-glial interactions
Rats
Retina
Retina - metabolism
Science
Science (multidisciplinary)
Thymidine
Transcription activation
Transcription factors
Transcription Factors - metabolism
Zebrafish
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Summary:Retinal Müller glia have a capacity to regenerate neurons in lower vertebrates like zebrafish, but such ability is extremely limited in mammals. In zebrafish, Müller glia proliferate after injury, which promotes their neurogenic reprogramming while inhibiting reactive gliosis. In mammals, however, how the cell cycle affects the fate of Müller glia after injury remains unclear. Here, we focused on the expression of proneural transcription factors, Ngn2 and Ascl1, and a gliosis marker glial fibrillary acidic protein (GFAP) in rat Müller glia after N -methyl- N -nitrosourea (MNU)-induced photoreceptor injury and analyzed the role of Müller glia proliferation in the regulation of their expression using retinal explant cultures. Thymidine-induced G1/S arrest of Müller glia proliferation significantly hampered the expression of Ascl1, Ngn2, and GFAP, and release from the arrest induced their upregulation. The migration of Müller glia nuclei into the outer nuclear layer was also shown to be cell cycle-dependent. These data suggest that, unlike the situation in zebrafish, cell cycle progression of Müller glia in mammals promotes both neurogenic reprogramming and reactive gliosis, which may be one of the mechanisms underlying the limited regenerative capacity of the mammalian retina.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-023-50222-0