Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy

查看全文 作　　者：LIU [1]Jin;YEUNG Patrick Ka [1]Kit;CHENG [1]Lu;LO Amy Cheuk [2,3]Yin;CHUNG Stephen Sum [4]Man;CHUNG Sookja [1,3,5]Kim

机构地区：[1]Department of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong;[2]Department of Ophthalmology, Li Ka Shing Faculty of Medicine, The University of Hong Kong;[3]Research Centre of Heart, Brain, Hormone and Healthy Aging, Li Ka Shing Faculty of Medicine, The University of Hong Kong;[4]Division of Science and Technology, United International College, Zhuhai 519085, China;[5]State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong

出　　处：《Science China(Life Sciences)》索引2015年第58卷第6期,共10页

基　　金：supported by the Research Grants Council of Hong Kong(RGC)HKU 764008M to Sookja Kim Chung 摘　　要：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. 关键词：视网膜神经节细胞缺血/再灌注损伤氧化应激神经胶质细胞反应缺乏症闭塞病变

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Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy

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