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Y. Ozawa, K. Nakao, T. Kurihara, T. Shimazaki, S. Shimmura, S. Ishida, A. Yoshimura, K. Tsubota, H. Okano; SOCS3 Is Required to Protect Photoreceptor Cell Function During Retinal Inflammation. Invest. Ophthalmol. Vis. Sci. 2008;49(13):943.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the role of suppressor of cytokine signaling 3 (SOCS3), an intracellular, ligand-induced negative feedback modulator of STAT3 activation, in the photoreceptor cell protection during retinal inflammation. We have previously reported that SOCS3 is required for the onset of photoreceptor cell differentiation and Rhodopsin expression in the perinatal retina. Here, we demonstrate an important role of SOCS3 in the adult retina during inflammation.
SOCS3-deficient and wild-type adult mice were intraperitoneally injected with Lipoplysaccaride (LPS) to induce retinal inflammation. Expression of SOCS3 and activated STAT3 in the adult retinas were analyzed immunohistochemistry. STAT3 activation and Rhodopsin expression were measured by immunoblot analysis 8 and 48 hours, and 10 days after LPS injection. Electroretinogram (ERG) was recorded 10 days after LPS injection.
SOCS3 was expressed in the photoreceptor cells in the adult retinas. During inflammation, STAT3 activation was more intensive in the SOCS3-deficient mice especially in the photoreceptor cells. Concomitantly, Rhodopsin expression during retinal inflammation was decreased also in the wild-type mice but more rapidly and profoundly in the SOCS3-deficient mice. Decrease of a-wave amplitude in ERG was prolonged and still observed 10 days after LPS injection only in the SOCS3-deficient mice.
SOCS3 is required to inhibit excessive STAT3 activation and minimize the decrease in Rhodopsin. SOCS3 contributes to protect visual function during retinal inflammation.
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