Kim Jeong Hun, Yu Young Suk, Kim Jin Hyoung, Kim Kyu-Won, Min Bon-Hong
Department of Ophthalmology, Seoul National University College of Medicine, & Seoul Artificial Eye Center, Clinical Research Institute, Seoul National University Hospital, Seoul, Korea.
Curr Eye Res. 2007 Jul-Aug;32(7-8):693-8. doi: 10.1080/02713680701487871.
Clusterin has been reported to be up-regulated in diverse pathophysiological stresses, but its role is controversial. In this study, we investigated the role of clusterin under in vitro ischemia of human retinal endothelial cells (HRECs). When HRECs were exposed to oxygen-glucose deprivation (OGD), clusterin expression increased, whereas von Willebrand factor (vWF), occludin, and zonula occludens (ZO-1) markedly decreased. Interestingly, loss of tight junction proteins and death of HRECs in OGD conditions were restored by clusterin treatment. Our results suggest that the enhanced clusterin in OGD conditions may play a protective role against ischemia-induced tight junction protein loss and HRECs death.
据报道，在多种病理生理应激中，簇集蛋白表达上调，但其作用存在争议。在本研究中，我们调查了簇集蛋白在人视网膜内皮细胞（HRECs）体外缺血情况下的作用。当HRECs暴露于氧糖剥夺（OGD）时，簇集蛋白表达增加，而血管性血友病因子（vWF）、闭合蛋白和紧密连接蛋白1（ZO-1）明显减少。有趣的是，通过簇集蛋白处理可恢复OGD条件下紧密连接蛋白的丢失及HRECs的死亡。我们的结果表明，OGD条件下增强的簇集蛋白可能对缺血诱导的紧密连接蛋白丢失和HRECs死亡起到保护作用。
