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.
Bibliographical noteFunding Information:
This work was supported by 03-2004-0200 from the Seoul National University Hospital Research Fund and by grant no. R01-2004-000-10212-0 from the Basic Research Program of the Korea Science and Engineering Foundation.
- Endothelial cells
- Protective role
- Tight junction proteins
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience