Requirement for Generation of H <sub>2</sub> O <sub>2</sub> for Platelet-Derived Growth Factor Signal Transduction

  • Maitrayee Sundaresan
    Cardiology Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD 20892-1650, USA.
  • Zu-Xi Yu
    Pathology Section, NHLBI, NIH, Bethesda, MD 20892-1518, USA.
  • Victor J. Ferrans
    Pathology Section, NHLBI, NIH, Bethesda, MD 20892-1518, USA.
  • Kaikobad Irani
    Cardiology Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD 20892-1650, USA.
  • Toren Finkel
    Cardiology Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD 20892-1650, USA.

抄録

<jats:p> Stimulation of rat vascular smooth muscle cells (VSMCs) by platelet-derived growth factor (PDGF) transiently increased the intracellular concentration of hydrogen peroxide (H <jats:sub>2</jats:sub> O <jats:sub>2</jats:sub> ). This increase could be blunted by increasing the intracellular concentration of the scavenging enzyme catalase or by the chemical antioxidant <jats:italic>N</jats:italic> -acetylcysteine. The response of VSMCs to PDGF, which includes tyrosine phosphorylation, mitogen-activated protein kinase stimulation, DNA synthesis, and chemotaxis, was inhibited when the growth factor-stimulated rise in H <jats:sub>2</jats:sub> O <jats:sub>2</jats:sub> concentration was blocked. These results suggest that H <jats:sub>2</jats:sub> O <jats:sub>2</jats:sub> may act as a signal-transducing molecule, and they suggest a potential mechanism for the cardioprotective effects of antioxidants. </jats:p>

収録刊行物

  • Science

    Science 270 (5234), 296-299, 1995-10-13

    American Association for the Advancement of Science (AAAS)

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