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N. Katai, S. Arai-Gaun, T. Kikuchi, N. Yoshimura; Heme Oxygenase-1 is Essential to the Survival of Müller Cells after Ischemic Reperfusion Injury . Invest. Ophthalmol. Vis. Sci. 2003;44(13):457.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: We previously screened the gene expression profile in retinal ischemia reperfusion injury by using the DNA microarray system and discovered the opposite functional gene groups were expressed in injured retina. One is the cell death promoting genes expressing in dying retinal neurons and another is the cell death protecting genes in surviving cells. We focused on the latter one, especially Heme oxygenase-1 (HO-1). Our purpose is to characterize the HO-1 induced in Müller cells after ischemia reperfusion injury. Methods: Transient retinal ischemia for 45-60 minutes was performed to male Sprague-Dawley rats (200-300g) by increasing the intraocular pressure. Retinas were collected at various time points after reperfusion, and both protein and gene expression levels were measured by using Western blotting and real-time RT-PCR methods, respectively. Localization of HO-1 proteins in injured retina was determined using the immunohistochemical methods. To clarify the function of HO-1 in ischemic injured retina, the inhibitors of HO-1 were applied. Results: On Western blotting, HO-1 was induced in injured retina from 6 to 48 hours after ischemic insult but not in sham operated retina. The peak time point was at 12 hours to 24 hours after reperfusion. HO-1 gene expression level was gradually increased after the injury and the peak time point was at 12 hour after the ischemic insult. HO-1 was expressed only in Müller cells of all somata from the inner limiting membrane to the outer limiting membrane. Neuronal cells were not stained with anti-HO-1 antibody. After the treatment of HO-1 inhibitors, HO-1 expression was totally blocked. Müller cells were completely disappeared in some areas. In these areas, the architecture of retina was disrupted. Conclusions: HO-1 was only expressed in the Müller cell after the ischemia reperfusion injury. HO-1 was essentially needed for the survival of Müller cells in the ischemic retinal injury.
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