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您的检索式：作者名="YEUNG Patrick Ka Kit"
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| 1 | Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy显示文摘Ischemia occurs in diabetic retinopathy with neuronal loss, edema, glial cell reactivity and oxidative stress. Epacs, consisting of Epac1 and Epac2, are c AMP mediators playing important roles in maintenance of endothelial barrier and neuronal functions. To investigate the roles of Epacs in the pathogenesis of ischemic retinopathy, transient middle cerebral artery occlusion(t MCAO) was performed on Epac1-deficient(Epac1-/-) mice, Epac2-deficient(Epac2-/-) mice, and their wild type counterparts(Epac1+/+ and Epac2+/+). Two-hour occlusion and 22-hour reperfusion were conducted to induce ischemia/reperfusion injury to the retina. After t MCAO, the contralateral retinae displayed similar morphology between different genotypes. Neuronal loss, retinal edema and increase in immunoreactivity for aquaporin 4(AQP4), glial fibrillary acidic protein(GFAP), peroxiredoxin 6(Prx6) were observed in ipsilateral retinae. Epac2-/- ipsilateral retinae showed more neuronal loss in retinal ganglion cell layer, increased retinal thickness and stronger immunostaining of AQP4, GFAP, and Prx6 than those of Epac2+/+. However, Epac1-/- ipsilateral retinae displayed similar pathology as those in Epac1+/+ mice. Our observations suggest that Epac2-deficiency led to more severe ischemic retinopathy after retinal ischemia/reperfusion injury. | LIU Jin YEUNG Patrick Ka Kit CHENG Lu LO Amy Cheuk Yin CHUNG Stephen Sum Man CHUNG Sookja Kim | 2015 | Science China(Life Sciences)2015，58，6： | 12 |
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