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  • Title: ICAM-1 and p38 MAPK mediate fibrinogen-induced migration of human vascular smooth muscle cells.
    Author: Rauch BH, Müschenborn B, Braun M, Weber AA, Schrör K.
    Journal: Eur J Pharmacol; 2007 Dec 22; 577(1-3):54-7. PubMed ID: 17904546.
    Abstract:
    Fibrinogen deposition in the vessel wall represents an independent atherogenic risk factor. In Boyden-chamber assays, fibrinogen concentration-dependently (1-100 microM) induced migration of human vascular smooth muscle cells (SMC). This was inhibited by antibodies to intercellular adhesion molecule-1 (ICAM-1, 10 microg/ml), and by inhibitors of PI3-kinase (LY294002, 10 microM) and MAPK (mitogen-activated protein kinase) p38 (SB203580, 10 microM). The MEK (MAP kinase kinase) inhibitor PD98059 (10 muM) and the GPIIb/IIIa antagonist abciximab (10 mug/ml) had no effect. ICAM-1 antibodies inhibited fibrinogen-induced Akt and p38 phosphorylation. Thus fibrinogen stimulates human SMC migration through binding to ICAM-1 and activation of Akt and p38.
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