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S. Gaun, N. Katai, K. Ohta, T. Kikuchi, N. Yoshimura; The Protective Effect of Heme Oxygenase–1 on Retinal Ischemia–Reperfusion Injury in Rats . Invest. Ophthalmol. Vis. Sci. 2004;45(13):3283.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: We previously screened the gene expression profile in retinal ischemia reperfusion by using a microarray system, and have shown that heme oxygenase–1 (HO–1), one of the cell protecting genes in survival cells, was expressed in Müller cells. The purpose of this study is to investigate possible roles of HO–1 in ischemia–reperfusion injury of the rat retina. Methods: Retinal ischemia was induced in male 8–week Sprague–Dawley rats by increasing the intraocular pressure to 110 mmHg for 60 minutes. At 12 and 24 hours after reperfusion, eyes were enucleated. To inhibit the up–regulation of HO–1, short interfering RNA (siRNA) of HO–1 was injected intravitreally before the ischemia. Protein expression levels of HO–1 and HO–2 were studied by using Western blotting at 12 and 24 hours after reperfusion. Müller cells was assessed by counting the number of s–100 positive cells, and the number of macrophages invading the retina was determined by counting the number of ED1–positive cells. Also, the production of oxidized proteins was analyzed by OxyBlot. Results: The HO–1 protein expression in the retina treated with HO–1 siRNA was suppressed at 12 and 24 hours. In HO–1 siRNA treated retina, a number of inflammatory cells infiltrated into the retina, and the retina become thin and folds were formed. The number of s–100 positive cells was decreased significantly in retinas treated with HO–1 siRNA. The number of infiltrating macrophages and oxidized proteins were increased in retinas pretreated with the siRNA of HO–1. Conclusions: HO–1 has cytoprotective effects on Müller cells and plays an anti–inflammatory, anti–oxidative role against the ischemia–reperfusion injury.
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