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

Several investigations have postulated evidence of the involvement of apopt osis in delayed neuronal death following brief periods of global cerebral i schemia. 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 fo lding and assembly within the mitochondria. This study investigated the ind uction of these mitochondrial stress protein genes in the hippocampal CAI r egion and less vulnerable regions following transient forebrain ischemia. I n situ hybridization analysis revealed that the induction pattern of HSP60 mRNA was identical to that of HSP10 mRNA throughout the entire ischelnic co urse. No changes occurred in the expression of both mRNAs after 2 min ische mia. Strong induction of both mRNAs occurred in the CAI region after 10 min ischemia and persisted until 1 d after I reperfusion. In contrast, inducti on of both mRNAs in the less vulnerable regions was terminated by 1 d after reperfusion. These results demonstrate that mitochondrial stress condition s persist concomitantly with cytosolic stress conditions in regions vulnera ble to transient forebrain ischemia. (C) 2000 Elsevier Science B.V. All rig hts reserved.