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 phospholipid 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 epitheliaal cells (BSC-1) was examined. Hsp70-mRNA expression was induced by hyperthermia (HT) (42°C, 60 min). Hsp70 protein accumulation was maximal after 12–18 h and returned to baseline levels by 96 h. Treatment of BSC-1 cells with ionomycin (7.0 µM) produced lethal cell injury characterized by LDH release. Cells examined at 18 h after HT were significantly less damaged than cells studied at 96 h after HT. Our data are the first to demonstrate that heat preconditioning confers protection from Ca²⁺-mediated cell injury. The state of increased tolerance is transient and closely parallels kinetics of Hsp70 expression.