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Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
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ICAM-1 and p38 MAPK mediate fibrinogen-induced migration of human vascular smooth muscle cells

Bernhard H Rauch1, Birgit Müschenborn, Marina Braun

  • 1Institut für Pharmakologie und Klinische Pharmakologie, Universitätsklinikum, Düsseldorf, Universitätsstr. 1, 40225 Düsseldorf, Germany.

European Journal of Pharmacology
|October 2, 2007
PubMed

Insights

Fibrinogen in vessel walls drives smooth muscle cell migration via intercellular adhesion molecule-1 (ICAM-1). This process involves activating PI3-kinase/Akt and MAPK p38 pathways, crucial for atherosclerosis development.

Area of Science:

  • Cardiovascular Biology
  • Atherosclerosis Research
  • Cellular Signaling

Background:

  • Vessel wall fibrinogen deposition is an independent risk factor for atherosclerosis.
  • Understanding the mechanisms of smooth muscle cell (SMC) migration is critical for preventing vascular disease.

Purpose of the Study:

  • To investigate the role of fibrinogen in inducing human vascular SMC migration.
  • To elucidate the molecular pathways and adhesion molecules involved in fibrinogen-mediated SMC migration.

Main Methods:

  • Boyden-chamber assays were used to measure human vascular SMC migration.
  • Experiments involved varying fibrinogen concentrations and utilizing specific inhibitors and antibodies.
  • Western blotting was employed to assess protein phosphorylation, including Akt and p38.

Main Results:

  • Fibrinogen dose-dependently induced human SMC migration.
  • Migration was inhibited by antibodies against intercellular adhesion molecule-1 (ICAM-1) and by PI3-kinase and p38 MAPK inhibitors.
  • ICAM-1 antibody treatment blocked fibrinogen-induced phosphorylation of Akt and p38.

Conclusions:

  • Fibrinogen stimulates human SMC migration by binding to ICAM-1.
  • This interaction activates the PI3-kinase/Akt and p38 MAPK signaling pathways.
  • Targeting the fibrinogen-ICAM-1 interaction may offer a therapeutic strategy for atherosclerosis.

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