HSP70 is essential to the neuroprotective effect of heat-shock.
Many kinds of injuries induce 72 kDa heat-shock protein (HSP70) in the central nervous system. We investigated the role of HSP70 in promoting the survival of rat hippocampal neurons in primary culture. Heat-shock (42 degrees C for 30 min) significantly increased the number of surviving neurons independently of the initial density of plated cells, suggesting a direct effect on the neurons. Immunohistochemical detection revealed that HSP70 was expressed in virtually all cells six hours after the heat-shock and the immunostaining became stronger during the observation period of 72 h. HSP70 immunoreactivity was localized in the nucleus at 24 h after the heat-shock, but was diffused throughout the cytoplasm at 72 h. Addition of an antisense oligonucleotide to the medium significantly suppressed the neuroprotective effect of the heat-shock to control level, while a sense oligonucleotide had no effect. HSP70 immunoreactivity was completely abolished in the presence of the antisense oligonucleotide. These results indicate that HSP70 is essential for neuroprotection by heat-shock.
Sato
K
K
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Saito
H
H
Matsuki
N
N
D000818:Animals; D002470:Cell Survival / Q000502:physiology*; D002478:Cells, Cultured; D018840:HSP70 Heat-Shock Proteins / Q000502:physiology*; D006624:Hippocampus / Q000502:physiology*; D007150:Immunohistochemistry; D018696:Neuroprotective Agents / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar
D018840:HSP70 Heat-Shock Proteins; D018696:Neuroprotective Agents