Inhibition of NADH/NADPH oxidase affects signal transduction by growth factor receptors in normal fibroblasts

Arch Biochem Biophys. 2002 Jan 15;397(2):253-7. doi: 10.1006/abbi.2001.2641.

Abstract

Reactive oxygen species have been implicated as possible second messengers in mitogenic signal transduction. We demonstrate that in normal fibroblasts the treatment with the two inhibitors of phagocytic NADH/NADPH oxidase prevents tyrosine phosphorylation of platelet-derived growth factor receptor upon the exposure of serum-deprived cells to growth factors. Furthermore, the inhibition of NADH/NADPH oxidase abolishes ERKs activation and p21(waf1) accumulation that occurs when cells are exposed to growth factors. Finally, NADH/NADPH inhibitors prevent the p66(Shc) Ser-phosphorylation induced by serum and by phorbol 12-myristate-13-acetate, which suggests that the direct target(s) of reactive oxygen species is(are) located upstream from the machinery connecting growth factor receptors to Ras.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcysteine / pharmacology
  • Animals
  • Blood
  • Culture Media
  • Enzyme Inhibitors / pharmacology
  • Fibroblasts / cytology
  • Fibroblasts / metabolism
  • NADH, NADPH Oxidoreductases / antagonists & inhibitors
  • NADH, NADPH Oxidoreductases / metabolism*
  • Onium Compounds / pharmacology
  • Rats
  • Receptors, Growth Factor / metabolism*
  • Signal Transduction
  • Sulfones / pharmacology

Substances

  • Culture Media
  • Enzyme Inhibitors
  • Onium Compounds
  • Receptors, Growth Factor
  • Sulfones
  • 4-(2-aminoethyl)benzenesulfonylfluoride
  • diphenyleneiodonium
  • NADH, NADPH Oxidoreductases
  • Acetylcysteine