HEAT-PRECONDITIONING CONFERS PROTECTION FROM CA2-MEDIATED CELL TOXICITY IN RENAL TUBULAR EPITHELIAL-CELLS (BSC-1)()

A rise in intracellular calcium may mediate ischemic damage by phospho lipid hydrolysis and proteolysis. Heat shock proteins have been shown to provide protection from various forms of cell stress, but not from models of Ca2+-mediated injury. The effect of heat preconditioning in a model of ionomycin-induced injury in cultured renal tubular epitheli al cells (BSC-1) was examined. Hsp70-mRNA expression was induced by hy perthermia (HT) (42 degrees C, 60 min). Hsp70 protein accumulation was maximal after 12-18 h and returned to baseline levels by 96 h. Treatm ent of BSC-I cells with ionomycin (7.0 mu M) produced lethal cell inju ry characterized by LDH release. Cells examined at 18 h after HT were significantly less damaged than cells studied at 96 h after HT. Our da ta are the first to demonstrate that heat preconditioning confers prot ection from Ca2+-mediated cell injury. The state of increased toleranc e is transient and closely parallels kinetics of Hsp70 expression.