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J. Arai, N. Katai, K. Kuida, N. Yoshimura; Caspase-1 Deficient Mice Were Rescued from Apoptosis of the Retinal Neuronal Cells by Ischemia-reperfusion . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2922.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: We have shown that caspase-1 (ICE) plays a role in mice photoreceptor cells apoptosis by excessive light exposure (ARVO meeting, 2001). ICE was suggested also to play an important role in retinal ischemia-reperfusion injury. In this study, we investigated whether caspase-1 perticipates apoptosis of photoreceptor cells after an ischemia-reperfusion injury. Methods: Retinal ischemia was induced in 8-10 week old ICE deficient (ICE(-/-)) and wild type (C57BL/6) mice by raising the intraocular pressure to 110 mm Hg for 45 minutes. Mice were killed with an overdose of sodium pentobarbital before and at 1, 2 and 14 days after reperfusion. The eyes were immediately enucleated and retinal neuronal apoptosis was evaluated by the TdT-dUTP terminal nick-end labeling (TUNEL) staining. Also morphometric evaluation of the inner retinal thickness at 2 weeks after the injury was done. Results: The number of TUNEL-positive cells in the inner nuclear layer at 1 day after reperfusion was decreased significantly in ICE (-/-) mice compared with that in the wild type mice (p<0.001). 14 days after reperfusion, the thickness of the inner retina of wild type and of ICE (-/-) were 29.6+/-6.4 microm and 35.5+/-8.9 microm, respectively (p < 0.05). Conclusions: Cell damage in the inner nuclear layer of caspase-1 deficient mice after the ischemia-reperfusion injury was significantly reduced compared to that in wild type mice. Caspase-1 plays an important role in the retinal neuronal apoptosis in ischemia-reperfusion injury.
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