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

Curr Eye Res. 2007 Jul-Aug;32(7-8):693-8. doi: 10.1080/02713680701487871.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Blood-Retinal Barrier / physiology
  • Blotting, Western
  • Cell Hypoxia
  • Cell Survival
  • Cells, Cultured
  • Chromatography, Affinity
  • Clusterin / pharmacology
  • Clusterin / physiology*
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / metabolism*
  • Glucose / deficiency
  • Humans
  • Indoles / metabolism
  • Ischemia / metabolism*
  • Membrane Proteins / metabolism
  • Occludin
  • Phosphoproteins / metabolism
  • Retinal Vessels / metabolism*
  • Staining and Labeling
  • Zonula Occludens-1 Protein
  • von Willebrand Factor / metabolism

Substances

  • CLU protein, human
  • Clusterin
  • Indoles
  • Membrane Proteins
  • OCLN protein, human
  • Occludin
  • Phosphoproteins
  • TJP1 protein, human
  • Zonula Occludens-1 Protein
  • von Willebrand Factor
  • DAPI
  • Glucose