論文

査読有り
2011年9月

Endoplasmic reticulum stress induces retinal endothelial permeability of extracellular-superoxide dismutase

FREE RADICAL RESEARCH
  • Tetsuo Adachi
  • ,
  • Hiroyuki Yasuda
  • ,
  • Shinsuke Nakamura
  • ,
  • Tetsuro Kamiya
  • ,
  • Hirokazu Hara
  • ,
  • Hideaki Hara
  • ,
  • Tsunehiko Ikeda

45
9
開始ページ
1083
終了ページ
1092
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3109/10715762.2011.595408
出版者・発行元
INFORMA HEALTHCARE

The aim of this study was to determine the reasons why the intravitreal level of extracellular-superoxide dismutase (EC-SOD) increases in proliferative diabetic retinopathy patients by the investigation of two possibilities: first, change of EC-SOD expression in the retina; and secondly, leakage of EC-SOD through the endothelial monolayer by the treatment with endoplasmic reticulum (ER) stress inducers because ER stress is known to be involved in the vascular impairment in diabetic retinopathy. Intravitreous injection of tunicamycin in mice increased the permeability of tracer dye across retinal blood vessels while the retinal EC-SOD mRNA level was not changed. The leakage of EC-SOD through the retinal endothelial cell layer was elevated by the treatment with thapsigargin or tunicamycin. The expression of claudin-5 was significantly decreased by the treatment with the ER stress inducers. These phenomena were significantly suppressed by the pretreatment of endothelial cells with a chemical chaperone 4-phenylbutyric acid. Our observations suggest that ER stress leads to the down-regulation of claudin-5 among tight junction proteins and may induce the elevation of endothelial permeability and leakage of EC-SOD into the vitreous body.

Web of Science ® 被引用回数 : 21

リンク情報
DOI
https://doi.org/10.3109/10715762.2011.595408
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/21736484
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000293542300010&DestApp=WOS_CPL