埃兹蛋白磷酸化参与缺血/再灌注诱导的视网膜内血视网膜屏障功能障碍。
Involvement of moesin phosphorylation in ischemia/reperfusion induced inner blood-retinal barrier dysfunction.
作者信息
Xu Jing, Liu Qiong, Ma Ming, Chen Lin-Jiang, Yu Jian, Xiong Ke, Wu Jing
机构信息
Department of Ophthalmology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong Province, China.
Huiqiao Medical Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong Province, China.
出版信息
Int J Ophthalmol. 2020 Apr 18;13(4):545-551. doi: 10.18240/ijo.2020.04.03. eCollection 2020.
AIM
To investigate the role of moesin and its underlying signal transduction in retinal vascular damage induced by retinal ischemia-reperfusion (RIR) insult.
METHODS
C57BL/6 mice were subjected to continued ischemia for 45min, followed by blood reperfusion. The expression and phosphorylation of moesin in retinal vessels were detected by immunohistochemistry and Western blotting. The inner blood-retinal barrier was evaluated using FITC-dextran leakage assay on whole-mount retina. Further studies were conducted to explore the effects of p38 mitogen-activated protein kinase (MAPK) pathway on the involvement of moesin in RIR-evoked retinal vascular hyperpermeability response.
RESULTS
It revealed that RIR induced moesin phosphorylation in a time-dependent manner after reperfusion. The phosphorylation of moesin was alleviated by inhibitions of p38 MAPK, while this treatment also ameliorated the dysfunction of inner blood-retinal barrier.
CONCLUSION
The results suggest that moesin is involved in RIR-evoked retinal vascular endothelial dysfunction and the phosphorylation of moesin is triggered p38 MAPK activation.
目的
探讨埃兹蛋白（moesin）及其潜在信号转导在视网膜缺血再灌注（RIR）损伤诱导的视网膜血管损伤中的作用。
方法
对C57BL/6小鼠进行45分钟的持续缺血，随后进行血液再灌注。通过免疫组织化学和蛋白质印迹法检测视网膜血管中埃兹蛋白的表达和磷酸化。使用FITC-葡聚糖渗漏试验在全层视网膜上评估内血视网膜屏障。进一步研究探讨p38丝裂原活化蛋白激酶（MAPK）通路对埃兹蛋白参与RIR诱发的视网膜血管高通透性反应的影响。
结果
结果显示，再灌注后RIR以时间依赖性方式诱导埃兹蛋白磷酸化。抑制p38 MAPK可减轻埃兹蛋白的磷酸化，同时该处理也改善了内血视网膜屏障的功能障碍。
结论
结果表明，埃兹蛋白参与RIR诱发的视网膜血管内皮功能障碍，且埃兹蛋白的磷酸化由p38 MAPK激活触发。
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