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Mercy D Pawar, Boris Busov, Jingyu Yao, Qiong-Duon Zheng, David N Zacks, Cagri G Besirli; Fas Apoptotic Inhibitory Molecule 2 (Faim2) prevents retinal detachment induced photoreceptor apoptosis. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1117.
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© ARVO (1962-2015); The Authors (2016-present)
To test the role of Fas Apoptotic Inhibitory Molecule 2 (Faim2), an intrinsic inhibitor of the Fas death receptor apoptotic pathway, on photoreceptor survival after retinal detachment.
Retina-retinal pigment epithelium (RPE) separation was created in wild type and Faim2 knockout mice by subretinal injection of 1% hyaluronic acid. Level of Faim2 expression was determined in attached and detached retinas by Western blotting. Cell-specific expression of Faim2 was analyzed by immunohistochemistry. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) was performed in wild type and Faim2 knockout retinal sections 1, 3 and 7 days after retina-RPE separation. Photoreceptor survival was quantified in wild type and Faim2 knockout retinas 1 and 2 months after experimental detachment.
Retinal detachment led to rapid increase in Faim2 expression, which was primarily detected in the outer nuclear layer. Compared to wild type animals, Faim2 knockout mice showed increased TUNEL staining of the photoreceptors. Outer nuclear layers of Faim2 knockout retinas were thinner and had decreased number of photoreceptor nuclei 1 and 2 months post-detachment compared with retinas in wild type animals.
Expression of Faim2 protects photoreceptors from retinal-detachment induced, Fas-mediated apoptosis.
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