論文

査読有り
2000年

A pathway of neuronal apoptosis induced by hypoxia/reoxygenation: Roles of nuclear factor-κB, and Bcl-2

Journal of Neurochemistry
  • Michio Tamatani
  • ,
  • Noriaki Mitsuda
  • ,
  • Hideo Matsuzaki
  • ,
  • Haruo Okado
  • ,
  • Shin-Ichi Miyake
  • ,
  • Michael P. Vitek
  • ,
  • Atsushi Yamaguchi
  • ,
  • Masaya Tohyama

75
2
開始ページ
683
終了ページ
693
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1046/j.1471-4159.2000.0750683.x

As a model of the reperfusion injury found in stroke, we have exposed neurons to hypoxia followed by reoxygenation. Neurons treated with hypoxia/reoxygenation (H/R) respond by activating nuclear factor-κB (NFκB), releasing cytochrome c from their mitochondria, and ultimately dying. Further supporting an apoptotic mechanism, expression of the antiapoptotic Bcl-2 and Bcl-x proteins was increased following H/R. In this model, adenoviral- mediated transduction of IκB expression inhibited NFκB activation and significantly accelerated cytochrome c release and caspase-dependent neuronal death. At the same time, expression of mutated IκB prevented the increased expression of endogenous Bcl-2 and Bcl-x. In the presence of mutated IκB, singular overexpression of only Bcl-2 by adenoviral-mediated transduction significantly inhibited cytochrome c release, caspase-3-like activation, and cell death in response to H/R. These findings suggest a pathway where NFκB activation induces overexpression of Bcl-2 and Bcl-x, which function to prevent apoptotic cell death following H/R treatments.

リンク情報
DOI
https://doi.org/10.1046/j.1471-4159.2000.0750683.x
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/10899943
ID情報
  • DOI : 10.1046/j.1471-4159.2000.0750683.x
  • ISSN : 0022-3042
  • PubMed ID : 10899943
  • SCOPUS ID : 0033914534

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