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Travis J. Bailey, David R. Hyde; Role Of Endocytosis By Müller Glia During Photoreceptor Regeneration In The Zebrafish Retina. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2675.
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Unlike mammals, zebrafish can regenerate any neuronal cell type in the severely damaged retina. During regeneration of the light-damaged zebrafish retina, many, but not all of the Müller glia respond by proliferating to produce regenerative progenitor cells. Although the responding Müller glia seem to be in direct contact with apoptotic cells and engulf apoptotic debris, the molecular pathway(s) that trigger Müller glia to respond to damage is unknown. We tested whether clathrin-dependent or independent endocytosis facilitates this Müller glial proliferative response.
The eyes of light-damaged zebrafish were intravitreally injected with control saline, with or without an inhibitor of clathrin dependent-endocytosis (chlorpromazine), and were analyzed for cell death, by TUNEL, and proliferation, by immunohistochemistry. The effects of chlorpromazine treatment on expression of ascl1a and stat3, early upregulated markers of the Müller glial response, were also tested by quantitative real-time PCR.
Injection of chlorpromazine did not affect cell death in light-damaged retinas compared to saline-injected controls. Chlorpromazine-injected retinas showed reduced numbers of proliferating Müller glial cells relative to controls. The expression ascl1a and stat3 was also inhibited in chlorpromazine-treated retinas treated compared to saline controls.
This study suggests that clathrin-mediated endocytosis is required early in the regeneration response for the full complement of Müller glial cells to be activated.
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