Heat shock protein 70 overexpression protects LLC-PK1 tubular cells from heat shock but not hypoxia

Background. Overexpression of the 70 kDa heat shock protein (Hsp70) protect s myocytes and neural cells from hypoxic injury. In contrast, Hsp70 inducti on in the kidney after ischemic or thermal preconditioning does not correla te well with protection from hypoxic injury. Herein, we directly tested if Hsp70 overexpression protects LLC-PK1 porcine tubular epithelial cells from hypoxic or thermal injury. Methods. LLC-PK1 cells were either cotransfected with an Hsp70 and a lucife rase expression vector or singly transfected with the luciferase expression vector. Loss of intracellular luciferase activity was used to assess injur y after exposure to hypoxia or hyperthermia and after recovery under normal growth conditions. Results. Overexpression of Hsp70 decreased loss of and improved restoration of intracellular luciferase activity in LLC-PK1 cells exposed to hyperther mia. In contrast, Hsp70 overexpression did not decrease the loss of or impr ove restoration of luciferase activity in cells exposed to hypoxia. Conclusions. These results suggest that Hsp70 overexpression is sufficient to protect LLC-PK1 proximal tubular cells from hyperthermia but is not suff icient for protection from hypoxia.