論文

査読有り
2010年12月

Regulation of extracellular-superoxide dismutase in rat retina pericytes

REDOX REPORT
  • Tetsuo Adachi
  • ,
  • Hiroyuki Yasuda
  • ,
  • Kazunari Aida
  • ,
  • Tetsuro Kamiya
  • ,
  • Hirokazu Hara
  • ,
  • Ken-ichi Hosoya
  • ,
  • Tetsuya Terasaki
  • ,
  • Tsunehiko Ikeda

15
6
開始ページ
250
終了ページ
258
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1179/135100010X12826446921662
出版者・発行元
MANEY PUBLISHING

Diabetic retinopathy (DR) is regarded as a disease of the retinal microvascular system and metabolic abnormalities that are characteristic of oxidative stress and endoplasmic reticulum (ER) stress have been identified in the retina. Pericytes are known to be susceptible to oxidative stress and selective dropout of pericytes is one of the earliest pathological changes in DR. Extracellular-superoxide dismutase (EC-SOD) is a major antioxidative enzyme and protects vascular cells from the damaging effects of superoxide. Treatment with own conditioned medium significantly decreased EC-SOD expression in pericytes, while the expression of vascular endothelial growth factor and tumor necrosis factor-alpha were elevated. The addition of chemical chaperone 4-phenyl butyric acid significantly suppressed the effects of conditioned medium on EC-SOD and GRP78, a prominent ER-resident chaperone. Moreover, the cell viability of pericytes changed in a manner similar to that of EC-SOD expression. These results suggest that the expressions of EC-SOD should be regulated, at least partially, through ER stress. Continuous flow of culture media neutralized the ER-stress triggered decrease of EC-SOD expression. The stagnation of factors related to ER-stress around pericytes might reduce EC-SOD expression under pathophysiological conditions such as retinal edema, and this could induce and/or promote the intraretinal microvascular impairment and development of pathogenesis in DR.

Web of Science ® 被引用回数 : 9

リンク情報
DOI
https://doi.org/10.1179/135100010X12826446921662
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/21208524
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000285869300003&DestApp=WOS_CPL