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Bing Ross, Jingyu Yao, Sumathi Shanmugam, Steven Abcouwer, David N Zacks; Characterization of the Response of Microglia in a Rodent Model of Retinal Detachment . Invest. Ophthalmol. Vis. Sci. 2017;58(8):5378.
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© ARVO (1962-2015); The Authors (2016-present)
Retinal detachment (RD) causes a delayed apoptotic death of photoreceptors (PRs) and can trigger the activation of components of the immune system. The mechanism involved in the shifting of the PRs from survival to death following RD remains obscure and the role of microglia in this process is unknown. The purpose of this study was to examine the response of retinal microglia to RD.
C57BL/6 mice were sub-retinally injected with 1% hyaluronic acid to create an acute RD model. Immunohistochemistry (IHC) with antibodies to Iba1 and Ki67 on retinal whole mounts was used to evaluate the morphology and proliferation of microglia after RD. Flow cytometry with CD45, CD11b, Ly6C and Ly6G markers was used to quantify the number of microglia. IHC on 30 µm thick retinal sections was used to identify the location and migration of microglia in the retina.
RD promptly induced loss of process ramification and soma enlargement of microglia in detached retina, indicating activation. The appearance of Ki67 antigen indicated microglia entering the cell cycle at 2 days post RD. Total number of microglia was significantly increased at 3 days after RD. Furthermore, migration of microglia from the inner retinal layers into the outer nuclear layer was observed at 2 days following RD.
Retinal detachment induces the activation, proliferation, and migration of microglia from the inner retina towards the PRs. Microglia may therefore play important roles in PR survival and death after retinal detachment.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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