Adding complexity to fibronectin-platelet interactions.

The article by Chauhan et al in the current issue of Arteriosclerosis, Thrombosis, and Vascular Biology1 adds a new complexity to the roles of fibronectin in formation of hemostatic plugs and thrombotic occlusions. Normal mice, in which 99.5% of plasma fibronectin lacks the alternatively spliced EDA domain, were compared with mice genetically engineered to have only EDA-containing (EDA ) fibronectin in the circulation. Mice with only EDA fibronectin developed occlusive platelet thrombi more quickly in arterioles damaged by ferric chloride and suffered increased mortality from pulmonary emboli after an infusion of collagen and epinephrine in the tail vein. When blood from the 2 types of mice was passed through a collagen-coated chamber, surface coverage by adherent platelets was greater in the mice with EDA fibronectin. Examination of the photomicrographs suggests that the volume of platelet thrombi in the collagen-coated chamber also was greater after perfusion of blood from mice with EDA fibronectin. Three different read-outs, therefore, indicate that thrombus build-up is enhanced by the presence of EDA fibronectin,