Fibrinogen: a vascular risk factor, why? Contributing effect of oncostatin M on both fibrinogen biosynthesis by hepatocytes and participation in atherothrombotic risk related to modifications of endothelial cells.

Abstract

Fibrinogen is a vascular risk factor. We suggest that it is a marker of cytokine secretion that simultaneously stimulates fibrinogen biosynthesis and vascular modifications responsible for atherothrombosis. Among these cytokines, oncostatin M (OSM) is the most potent cytokine for inducing fibrinogen biosynthesis by hepatocytes, and it could contribute to endothelial cell anomalies involved in the atherothrombotic process. Here we show that OSM acts (1) by inducing the secretion involved in invasion of the vessel wall by monocytes; (2) by inducing angiogenesis it promotes plaque destabilization, rupture, and consequently thrombosis; and (3) by decreasing fibrinolysis on macrovascular endothelial cells.