File Download
  Links for fulltext
     (May Require Subscription)

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

TitleEpac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy
Authors
Issue Date2015
Citation
Science China Life Sciences, 2015, v.58 n. 6, p. 521-530 How to Cite?
AbstractIschemia 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.
Persistent Identifierhttp://hdl.handle.net/10722/218641

 

DC FieldValueLanguage
dc.contributor.authorLIU, J-
dc.contributor.authorYeung, PKK-
dc.contributor.authorCheng, L-
dc.contributor.authorLo, ACY-
dc.contributor.authorChung, SM-
dc.contributor.authorChung, SK-
dc.date.accessioned2015-09-18T06:49:08Z-
dc.date.available2015-09-18T06:49:08Z-
dc.date.issued2015-
dc.identifier.citationScience China Life Sciences, 2015, v.58 n. 6, p. 521-530-
dc.identifier.urihttp://hdl.handle.net/10722/218641-
dc.description.abstractIschemia 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.-
dc.languageeng-
dc.relation.ispartofScience China Life Sciences-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleEpac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy-
dc.typeArticle-
dc.identifier.emailYeung, PKK: ykkp@hkucc.hku.hk-
dc.identifier.emailCheng, L: lulu818@hku.hk-
dc.identifier.emailLo, ACY: amylo@hku.hk-
dc.identifier.emailChung, SK: skchung@hkucc.hku.hk-
dc.identifier.authorityLo, ACY=rp00425-
dc.identifier.authorityChung, SK=rp00381-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1007/s11427-015-4860-1-
dc.identifier.hkuros254462-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats