| Title | Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy |
| Creator | |
| Date Issued | 2015-06-20 |
| Source Publication | Science China Life Sciences
 |
| ISSN | 1674-7305 |
| Volume | 58Issue:6Pages:521-530 |
| Abstract | Ischemia occurs in diabetic retinopathy with neuronal loss, edema, glial cell reactivity and oxidative stress. Epacs, consisting of Epac1 and Epac2, are cAMP 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 (tMCAO) 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 tMCAO, 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. |
| Keyword | Epac ischemia retina retinopathy |
| DOI | 10.1007/s11427-015-4860-1 |
| URL | View source |
| Language | 英语English |
| Scopus ID | 2-s2.0-84931566593 |
| Citation statistics | |
| Document Type | Journal article |
| Identifier | http://repository.uic.edu.cn/handle/39GCC9TT/6450 |
| Collection | Beijing Normal-Hong Kong Baptist University |
| Corresponding Author | Chung，Sookja Kim |
| Affiliation | 1.Department of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong,Hong Kong,China 2.Department of Ophthalmology, Li Ka Shing Faculty of Medicine, The University of Hong Kong,Hong Kong,China 3.Research Centre of Heart, Brain, Hormone and Healthy Aging, Li Ka Shing Faculty of Medicine, The University of Hong Kong,Hong Kong,China 4.Division of Science and Technology, United International College,Zhuhai,519085,China 5.State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong,Hong Kong,China |
| Recommended Citation GB/T 7714 | Liu，Jin,Yeung，Patrick Ka Kit,Cheng，Luet al. Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy[J]. Science China Life Sciences, 2015, 58(6): 521-530. |
| APA | Liu，Jin, Yeung，Patrick Ka Kit, Cheng，Lu, Lo，Amy Cheuk Yin, Chung，Stephen Sum Man, & Chung，Sookja Kim. (2015). Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy. Science China Life Sciences, 58(6), 521-530. |
| MLA | Liu，Jin,et al."Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy". Science China Life Sciences 58.6(2015): 521-530. |
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