Stress-induced thermotolerance of the cytoskeleton of mouse neuroblastoma N2A cells and rat Reuber H35 hepatoma cells.
A conditioning treatment of 30 min at 42 degrees C or 43 degrees C, followed by a 4-h recovery period at 37 degrees C, induces thermotolerance state in the cytoskeleton of Reuber H35 hepatoma cells and N2A neuroblastoma cells. Evidence for the involvement of heat shock proteins in the development of thermotolerance in the cytoskeleton has been obtained from the following observations: only those conditioning treatments inducing the enhanced synthesis of heat shock proteins (HSPs) are able to induce the heat-resistant state of the cytoskeleton; prevention of HSP synthesis by actinomycin D or cycloheximide also prevents the acquisition of thermotolerance in the cytoskeleton; an alternative inducer of HSP synthesis, sodium arsenite, is also able to induce the cytoskeletal thermotolerance; the kinetics of development and disappearance of thermotolerance in the cytoskeleton is parallel to the kinetics of accumulation and decay of HSPs. The possible function of HSPs in the heat-resistant cytoskeleton of H35 hepatoma and N2A neuroblastoma cells is discussed.
D000818:Animals; D002478:Cells, Cultured; D003513:Cycloheximide / Q000494:pharmacology; D003599:Cytoskeleton / Q000648:ultrastructure*; D003609:Dactinomycin / Q000494:pharmacology; D006360:Heat-Shock Proteins / Q000096:biosynthesis*; D006358:Hot Temperature; D007700:Kinetics; D008114:Liver Neoplasms, Experimental / Q000648:ultrastructure; D051379:Mice; D009447:Neuroblastoma / Q000648:ultrastructure; D051381:Rats
D006360:Heat-Shock Proteins; D003609:Dactinomycin; D003513:Cycloheximide