論文

査読有り 国際誌
2012年9月15日

NADPH oxidase-mediated upregulation of connexin43 contributes to podocyte injury.

Free radical biology & medicine
  • Qiaojing Yan
  • ,
  • Kun Gao
  • ,
  • Yuan Chi
  • ,
  • Kai Li
  • ,
  • Ying Zhu
  • ,
  • Yigang Wan
  • ,
  • Wei Sun
  • ,
  • Hiroyuki Matsue
  • ,
  • Masanori Kitamura
  • ,
  • Jian Yao

53
6
開始ページ
1286
終了ページ
97
記述言語
英語
掲載種別
DOI
10.1016/j.freeradbiomed.2012.07.012

The gap junction protein connexin43 (Cx43) was markedly increased in podocytes in a rat model of nephrosis induced by puromycin. However, the mechanisms and roles of the altered Cx43 in podocytes are still unclear. Given that oxidative stress mediates podocyte injury under a variety of pathological situations, we examined the possible involvement of an oxidative stress-related mechanism in the regulation of Cx43. Incubation of podocytes with puromycin led to a time- and concentration-dependent loss of cell viability, which was preceded by an elevation in Cx43 levels. Concomitantly, puromycin also induced NOX4 expression and promoted superoxide (O(2)(·-)) generation. Inhibition of NADPH oxidase with apocynin and diphenyleneiodonium chloride or addition of the superoxide dismutase mimetic tempol completely abrogated, whereas the O(2)(·-) donors menadione and 2,3-dimethoxy-1,4-naphthoquinone reproduced, the effects of puromycin on Cx43 expression and cell injury. Further analysis demonstrated that treatment of podocytes with several structurally different gap-junction inhibitors significantly attenuated the cytotoxicity of puromycin. Our results thus indicate that NADPH oxidase-mediated upregulation of Cx43 contributes to podocyte injury.

リンク情報
DOI
https://doi.org/10.1016/j.freeradbiomed.2012.07.012
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/22824863
ID情報
  • DOI : 10.1016/j.freeradbiomed.2012.07.012
  • PubMed ID : 22824863

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