Heat shock protein hsp70 overexpression confers resistance against nitric oxide

FEBS Lett. 1996 Aug 5;391(1-2):185-8. doi: 10.1016/0014-5793(96)00730-2.

Abstract

Heat stress is known to render rat islet cells resistant against the toxic effects of nitric oxide, reactive oxygen intermediates and the islet cell toxin streptozotocin. We report here for the first time that protection against nitric oxide is mediated by the major heat shock protein, hsp70, even in the absence of heat stress. The human hsp70 gene was stably transfected into the rat insulinoma cell line RINm5F. Constitutive expression of hsp70 caused protection from NO-induced cell lysis which was of the same extent as seen after heat stressing cells. Our results identify hsp70 as a defence molecule against nitric oxide.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Cell Survival / drug effects
  • DNA Damage*
  • Drug Resistance
  • Gene Expression
  • HSP70 Heat-Shock Proteins / biosynthesis*
  • HSP70 Heat-Shock Proteins / physiology
  • Hot Temperature
  • Humans
  • Insulinoma
  • Kinetics
  • Nitric Oxide / toxicity*
  • Nitroprusside / toxicity*
  • Pancreatic Neoplasms
  • Protein Biosynthesis
  • Rats
  • Recombinant Proteins / biosynthesis
  • Transfection
  • Tumor Cells, Cultured

Substances

  • HSP70 Heat-Shock Proteins
  • Recombinant Proteins
  • Nitroprusside
  • Nitric Oxide