Heat shock proteins hsp90 and hsp70 protect neuronal cells from thermal stress but not from programmed cell death.
Prior exposure to a mild thermal stress can protect neuronal cells from a subsequent more severe stress including high temperature, ischemia, glutamate toxicity, or stimuli inducing apoptosis. Although the protective effect of thermal stress correlates with the elevated expression of the heat shock proteins (hsps), the protective effect of individual hsps has never been directly demonstrated in neuronal cells. Here we show that the constitutive overexpression of either of the major hsps, hsp90 or hsp70, can protect neuronal cells from thermal stress but not from stimuli that induce apoptosis. The possible mechanisms by which thermal stress can protect neuronal cells from apoptosis are discussed.
Mailhos
C
C
Department of Molecular Pathology, University College London Medical School, England.
Howard
M K
MK
Latchman
D S
DS
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D002478:Cells, Cultured; D005727:Ganglia, Spinal / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D018840:HSP70 Heat-Shock Proteins / Q000494:pharmacology*; D018841:HSP90 Heat-Shock Proteins / Q000494:pharmacology*; D006358:Hot Temperature; D009447:Neuroblastoma / Q000473:pathology; D009474:Neurons / Q000166:cytology* / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014162:Transfection; D014407:Tumor Cells, Cultured
D018840:HSP70 Heat-Shock Proteins; D018841:HSP90 Heat-Shock Proteins