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

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

doi:10.1080/02713680701487871

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

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

Research output: Contribution to journal › Article › peer-review

35 Citations (Scopus)

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.

Original language	English
Pages (from-to)	693-698
Number of pages	6
Journal	Current Eye Research
Volume	32
Issue number	7-8
DOIs	https://doi.org/10.1080/02713680701487871
Publication status	Published - 2007 Jul

Bibliographical note

Funding 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.

Keywords

Clusterin
Endothelial cells
Ischemia
Protective role
Tight junction proteins

ASJC Scopus subject areas

Ophthalmology
Sensory Systems
Cellular and Molecular Neuroscience

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10.1080/02713680701487871

Cite this

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title = "The role of clusterin in in vitro ischemia of human retinal endothelial cells",

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.",

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note = "Funding 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.",

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AU - Yu, Young Suk

AU - Kim, Jin Hyoung

AU - Kim, Kyu Won

AU - Min, Bon Hong

N1 - Funding 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.

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N2 - 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.

AB - 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.

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

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

Access to Document

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