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The role of clusterin in in vitro ischemia of human retinal endothelial cells

Cited 34 time in Web of Science Cited 34 time in Scopus
Authors

Kim, Jeong Hun; Yu, Young Suk; Kim, Jin Hyoung; Kim, Kyu-Won; Min, Bon-Hong

Issue Date
2007-09-14
Publisher
Taylor & Francis
Citation
Curr Eye Res. 2007 Jul-Aug;32(7-8):693-8.
Keywords
Apoptosis/drug effectsBlood-Retinal Barrier/physiologyBlotting, WesternCell HypoxiaCell SurvivalCells, CulturedChromatography, AffinityClusterin/pharmacology/*physiologyEndothelium, Vascular/drug effects/*metabolismGlucose/deficiencyHumansIndoles/metabolismIschemia/*metabolismMembrane Proteins/metabolismPhosphoproteins/metabolismRetinal Vessels/*metabolismStaining and Labelingvon Willebrand Factor/metabolism
Abstract
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.
ISSN
0271-3683 (Print)
Language
English
URI
http://www.informaworld.com/smpp/content~db=all?content=10.1080/02713680701487871

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17852194

https://hdl.handle.net/10371/15771
DOI
https://doi.org/10.1080/02713680701487871
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