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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:203-204
doi: 10.1161/ATVBAHA.107.159798
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:203.)
© 2008 American Heart Association, Inc.


Editorials

Adding Complexity to Fibronectin-Platelet Interactions

Deane F. Mosher

From the Departments of Biomolecular Chemistry and Medicine, University of Wisconsin-Madison.

Correspondence to Deane F. Mosher, Departments of Biomolecular Chemistry and Medicine, University of Wisconsin-Madison, 1300 University Avenue, Madison, Wisconsin 53706. E-mail dfmosher@wisc.edu


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

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,

See accompanying article on page 296

The increase in susceptibility to thrombi is even more remarkable when one considers concentrations of plasma fibronectin. Mice with 50% of normal plasma fibronectin have been shown previously to be protected from occlusive thrombi after arteriolar injury when compared with mice with 100% levels.2 Flow chamber experiments suggest that fibronectin concentrations below 50% normal are even more protective against thrombosis.3,4 The concentration of fibronectin in plasma of mice expressing the EDA+ variant was only 20% of . . . [Full Text of this Article]


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