Simultaneous induction of mitochondrial heat shock protein mRNAs in rat forebrain ischemia.
Brain Res Mol Brain Res
; 84(1-2): 127-34, 2000 Dec 08.
Article
em En
| MEDLINE
| ID: mdl-11113539
ABSTRACT
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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Isquemia Encefálica
/
Regulação da Expressão Gênica
/
Prosencéfalo
/
Proteínas de Choque Térmico
/
Mitocôndrias
Limite:
Animals
Idioma:
En
Revista:
Brain Res Mol Brain Res
Assunto da revista:
BIOLOGIA MOLECULAR
/
CEREBRO
Ano de publicação:
2000
Tipo de documento:
Article
País de afiliação:
Japão