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J-S Gwon, JI Moon, SJ Oh, JW Chung, MH Chun; The Upregulation Of Clusterin In The Rat Retina Following Transient Ischemia . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2196.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:Clusterin is a 70-85 kDa sulfated glycoprotein containing two nonidentical polypeptides of 40 kDa linked by disulfide bonds. Clusterin is shown to be upregulated in various pathological conditions of the brain including retina. This study was conducted to identify whether clusterin is upregulated and is correlated with apoptotic cell death in the ischemic rat retina. Methods:The intraocular pressure (IOP) was raised to 90-120 mmHg for 60 min, and the animals were sacrificed after 1 d, 3 d, 1 wk, 2 wk, and 4 wk of reperfusion. Immunocytochemistry and western blotting using anti-clusterin antisera were applied, and apoptotic cell death was determined by a modified TUNEL technique. Results:In the control retina, clusterin immunoreactivity was restricted to some profiles in the outer plexiform layer, inner nuclear layer and ganglion cell layer. Following ischemia and reperfusion, apparent immunoreactivity was visible in Müller cell up to 1 wk and its intensity reached a peak value at 3 d. however, from 2 wk onward, immunoreactivity was only visible in some photoreceptor cells. Quantitative evaluation by immunoblotting confirmed that clusterin expression showed a peak value at 3 d and then had declined again to 130% of controls at 4 wk postlesion. Double-labeling demonstrated that a few clusterin labeled cells also showed TUNEL-positivity. Conclusion:Our findings suggest that there might be causal relationship between clusterin expression and apoptotic cell death in the outer retina, and clusterin supplied by Müller cells might play an important role in the pathogeneis of damaged neurons following transient ischemia.
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