Simultaneous induction of mitochondrial heat shock protein mRNAs in rat forebrain ischemia

Atsuya Okubo, Hiroyuki Kinouchi, Yuji Owada, Hisanori Kunizuka, Hideaki Itoh, Kenji Izaki, Hisatake Kondo, Yohtalou Tashima, Takashi Yoshimoto, Kazuo Mizoi

研究成果: Article

21 被引用数 (Scopus)

抄録

Several investigations have postulated evidence of the involvement of apoptosis in delayed neuronal death following brief periods of global cerebral ischemia. Apoptosis may be closely linked to mitochondrial dysfunction. Heat shock protein (HSP) 60 and HSP10 are mitochondrial matrix proteins induced by stress and form the chaperonin complex that is implicated in protein folding and assembly within the mitochondria. This study investigated the induction of these mitochondrial stress protein genes in the hippocampal CA1 region and less vulnerable regions following transient forebrain ischemia. In situ hybridization analysis revealed that the induction pattern of HSP60 mRNA was identical to that of HSP10 mRNA throughout the entire ischemic course. No changes occurred in the expression of both mRNAs after 2 min ischemia. Strong induction of both mRNAs occurred in the CA1 region after 10 min ischemia and persisted until 1 d after reperfusion. In contrast, induction of both mRNAs in the less vulnerable regions was terminated by 1 d after reperfusion. These results demonstrate that mitochondrial stress conditions persist concomitantly with cytosolic stress conditions in regions vulnerable to transient forebrain ischemia. (C) 2000 Elsevier Science B.V.

元の言語English
ページ(範囲)127-134
ページ数8
ジャーナルMolecular Brain Research
84
発行部数1-2
DOI
出版物ステータスPublished - 2000 12 8

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience

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