論文

査読有り
2011年6月

ER stress inducer, thapsigargin, decreases extracellular-superoxide dismutase through MEK/ERK signalling cascades in COS7 cells

FREE RADICAL RESEARCH
  • Tetsuro Kamiya
  • ,
  • Aya Obara
  • ,
  • Hirokazu Hara
  • ,
  • Naoki Inagaki
  • ,
  • Tetsuo Adachi

45
6
開始ページ
692
終了ページ
698
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3109/10715762.2011.567985
出版者・発行元
INFORMA HEALTHCARE

It has been reported that tubular cells suffer an endoplasmic reticulum (ER) stress during the development of chronic kidney disease, which is a potent risk factor of cardiovascular disease. Moreover, under these conditions, reactive oxygen species are generated and induce cell injury. Extracellular-superoxide dismutase (EC-SOD) is a member of SODs and protects the cells from oxidative stress. Here, it is demonstrated that thapsigargin, an ER stress inducer, decreased EC-SOD expression, whereas the expression of Cu, Zn-SOD and Mn-SOD was not changed. On the other hand, another ER stress inducer, tunicamycin, did not affect the expression of EC-SOD. Further, it was shown that thapsigargin has the ability to activate extracellular-signal regulated kinase (ERK), but tunicamycin does not. Moreover, pre-treatment with U0126, an inhibitor of mitogen-activated protein kinase kinase (MEK)/ERK, suppressed thapsigargin-triggered EC-SOD reduction, suggesting that MEK/ERK signalling should play an important role in the regulation of EC-SOD in COS7 cells under ER stress conditions.

Web of Science ® 被引用回数 : 18

リンク情報
DOI
https://doi.org/10.3109/10715762.2011.567985
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/21417786
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000289631000006&DestApp=WOS_CPL