論文

査読有り 国際誌
2011年6月15日

Connexin43 hemichannels contribute to cadmium-induced oxidative stress and cell injury.

Antioxidants & redox signaling
  • Xin Fang
  • ,
  • Tao Huang
  • ,
  • Ying Zhu
  • ,
  • Qiaojing Yan
  • ,
  • Yuan Chi
  • ,
  • Jean X Jiang
  • ,
  • Peiyu Wang
  • ,
  • Hiroyuki Matsue
  • ,
  • Masanori Kitamura
  • ,
  • Jian Yao

14
12
開始ページ
2427
終了ページ
39
記述言語
英語
掲載種別
DOI
10.1089/ars.2010.3150

We investigated the potential involvement of connexin hemichannels in cadmium ions (Cd(2+))-elicited cell injury. Transfection of LLC-PK1 cells with a wild-type connexin43 (Cx43) sensitized them to Cd(2+)-elicited cell injury. The cell susceptibility to Cd(2+) was increased by depletion of glutathione (GSH) with DL-buthionine-[S,R]-sulfoximine, and decreased by N-acetyl-cysteine or glutathione reduced ethyl ester. Fibroblasts derived from Cx43 wild-type (Cx43+/+) and knockout (Cx43-/-) fetal littermates displayed different susceptibility to Cd(2+). Cd(2+) induced a higher concentration of reactive oxygen species, a stronger activation c-Jun N-terminal kinase, and significantly more severe cell injury in Cx43+/+ fibroblasts, as compared with Cx43-/- fibroblasts. Cd(2+) caused a reduction in intracellular GSH, whereas it elevated extracellular GSH. This effect of Cd(2+) was more dramatic in Cx43+/+ than Cx43-/- fibroblasts. Treatment of Cx43+/+ fibroblasts with Cd(2+) caused a Cx43 hemichannel-dependent influx of Lucifer Yellow and efflux of ATP. Collectively, our study demonstrates that Cx43 sensitizes cells to Cd(2+)-initiated cytotoxicity, possibly through hemichannel-mediated effects on intracellular oxidative status.

リンク情報
DOI
https://doi.org/10.1089/ars.2010.3150
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/21235398
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3096519
ID情報
  • DOI : 10.1089/ars.2010.3150
  • PubMed ID : 21235398
  • PubMed Central 記事ID : PMC3096519

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