The preconditioned hippocampus accelerates HSP70 heat shock gene expression following transient ischemia in the gerbil.
To evaluate the mechanism of tolerance for ischemia, inductions of heat shock protein (HSP) 70 mRNA and immunoreactive HSP70 protein were studied in the preconditioned gerbil hippocampus. Following the single 3.5-min ischemia, HSP70 mRNA was induced in all hippocampal cells. However, the hippocampal CA1 cells produced only a minimum HSP70 protein, and the cells were almost lost by 7 days. Following the 3.5-min ischemia after 2-min pretreatment, the CA1 cells produced a strong immunoreactive HSP70 signal and large populations of the CA1 cells survived at 7 days. The peak time of the HSP70 mRNA induction shifted to earlier period of reperfusion in the CA1 cells as compared to the case with single ischemia. This accelerated change of HSP70 expression could play an important role for the acquisition of ischemic tolerance of the hippocampal CA1 neurons.
Aoki
M
M
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Abe
K
K
Kawagoe
J
J
Nakamura
S
S
Kogure
K
K
D000222:Adaptation, Physiological; D000818:Animals; D015870:Gene Expression; D005849:Gerbillinae; D006360:Heat-Shock Proteins / Q000235:genetics*; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D002546:Ischemic Attack, Transient / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism
D006360:Heat-Shock Proteins; D012333:RNA, Messenger