Acrolein induces inflammatory response underlying endothelial dysfunction: a risk factor for atherosclerosis

Ann N Y Acad Sci. 2008 Apr;1126:185-9. doi: 10.1196/annals.1433.034.

Abstract

Endothelial dysfunction by proinflammatory stimuli represents an important link between risk factors and the pathologic mechanisms underlying atherosclerosis. Thus, control of the inflammatory status of endothelial cells is crucial to limiting the disease. Tobacco smoking induces inflammatory reactions and promotes atherosclerosis; however, the mechanism that links cigarette smoking to an increased incidence of atherosclerosis is poorly understood. Our study demonstrates that acrolein, a known toxin in tobacco smoke, elevates oxidative stress via inactivation of thioredoxin reductase and stimulates expression of cyclooxygenase-2 through activation of the protein kinase C, p38 mitogen-activated protein kinase, and cAMP response element-binding protein pathway in endothelial cells. Our finding suggests that acrolein may play a role in the progression of atherosclerosis.

MeSH terms

  • Acrolein / adverse effects*
  • Air Pollution / adverse effects
  • Atherosclerosis / epidemiology*
  • Cyclooxygenase 2 / biosynthesis
  • Cyclooxygenase 2 / genetics
  • Dinoprostone / biosynthesis
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / physiopathology*
  • Enzyme Induction
  • Humans
  • Inflammation / chemically induced*
  • Inflammation / complications
  • Lipid Peroxidation
  • Polyamines / adverse effects
  • Risk Factors
  • Smoking / adverse effects
  • Thioredoxin-Disulfide Reductase / antagonists & inhibitors

Substances

  • Polyamines
  • Acrolein
  • Cyclooxygenase 2
  • Thioredoxin-Disulfide Reductase
  • Dinoprostone