Muller glial cell reprogramming and retina regeneration
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TL;DR: In teleost fish, the response of Müller glia to retinal injury involves a reprogramming event that imparts retinal stem cell characteristics and enables them to produce a proliferating population of progenitors that can regenerate all major retinal cell types and restore vision.
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Abstract: Muller glia in the fish retina respond to injury by reprogramming to a stem-cell-like state that enables them to regenerate all of the major retinal cell types. Goldman reviews our current understanding of the mechanisms that regulate this regenerative response and considers how this knowledge might be applied to improve repair in the mammalian retina.
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Pharmacokinetic aspects of retinal drug delivery.
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Microglia in Retinal Degeneration.
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Single-cell transcriptomic atlas of the human retina identifies cell types associated with age-related macular degeneration.
Madhvi Menon,Shahin Mohammadi,Shahin Mohammadi,Jose Davila-Velderrain,Jose Davila-Velderrain,Brittany A. Goods,Tanina D. Cadwell,Yu Xing,Anat Stemmer-Rachamimov,Alex K. Shalek,J. C. Love,J. C. Love,Manolis Kellis,Manolis Kellis,Manolis Kellis,Brian P. Hafler +15 more
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References
Insulin and Fibroblast Growth Factor 2 Activate a Neurogenic Program in Müller Glia of the Chicken Retina
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The inhibitor of phagocytosis, O-phospho-L-serine, suppresses Müller glia proliferation and cone cell regeneration in the light-damaged zebrafish retina
TL;DR: O-phospho-l-serine (L-SOP), a molecule that mimics the phosphatidylserine head group and partially blocks microglial phagocytosis of apoptotic cells, disrupts Müller glia proliferation subsequent to or in parallel with ascl1a and stat3 activation, suggesting that at least one signaling mechanism is required to activate Müllerglia proliferation in the light-damaged retina.