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Lipid oxidation products and oxidized low-density lipoproteins impair platelet-derived growth factor receptor

Cecile Vindis1, Isabelle Escargueil-Blanc, Koji Uchida

  • 1INSERM U-466 and Biochemistry Department, IFR-3 1, CHU Rangueil, Toulouse, France.

Redox Report : Communications in Free Radical Research
|February 1, 2007
PubMed

Insights

Oxidized LDLs and 4-HNE impair platelet-derived growth factor receptor-beta (PDGFRbeta) signaling in vascular smooth muscle cells. This inhibition, linked to oxidative stress, may destabilize vulnerable plaques.

Area of Science:

  • Cardiovascular Biology
  • Cell Signaling
  • Atherosclerosis Research

Background:

  • Vascular smooth muscle cell (SMC) migration and proliferation are regulated by platelet-derived growth factor receptor-beta (PDGFRbeta) signaling.
  • Oxidized low-density lipoproteins (oxLDLs) and 4-hydroxynonenal (4-HNE) are implicated in vascular pathologies.

Purpose of the Study:

  • To investigate the dual effect of oxLDLs and 4-HNE on PDGFRbeta signaling in SMCs.
  • To determine the role of oxidative stress in PDGFRbeta regulation and its implications for plaque stability.

Main Methods:

  • Short-term and long-term incubation of SMCs with oxLDLs and 4-HNE.
  • Assessment of PDGFRbeta phosphorylation and HNE-PDGFR adduct formation.
  • In vivo studies using apoE-deficient mice and treatment with hydralazine (carbonyl scavenger).

Main Results:

  • Short-term exposure activated PDGFRbeta signaling.
  • Long-term exposure led to PDGFRbeta desensitization and inhibited phosphorylation.
  • Increased HNE-PDGFR adducts were observed in SMCs and in vivo, correlating with PDGFRbeta inhibition.
  • Hydralazine prevented PDGFRbeta inhibition both in vitro and in vivo.

Conclusions:

  • PDGFRbeta is a direct target of 4-HNE, acrolein, and oxidative stress.
  • Progressive PDGFRbeta inhibition contributes to defective SMC proliferation.
  • Inhibition of PDGFRbeta signaling may decrease the stability of vulnerable atherosclerotic plaques.

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