Reduced Plasma Fibronectin Leads to Delayed Thrombus Growth in the Injured Arterioles in Vivo
| Autor: | Jana Matuskova, Denisa D. Wagner, Crystal L. Piffath, Béatrice Cambien |
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| Rok vydání: | 2004 |
| Předmět: | |
| Zdroj: | Blood. 104:2619-2619 |
| ISSN: | 1528-0020 0006-4971 |
| DOI: | 10.1182/blood.v104.11.2619.2619 |
| Popis: | In addition to von Willebrand factor and fibrinogen, plasma fibronectin (pFN) contributes significantly to thrombus development in arteries. Complete deficiency of plasma fibronectin (in pFN conditional knockout mice) affects thrombus formation and growth and subsequent occlusion of injured arterioles in vivo. We wanted to study a more physiological decrease of plasma fibronectin without having to induce interferon production in the mice to excise the FN gene. Reduced pFN levels are common in patients with liver disease, sepsis and following trauma or surgery. To evaluate the effect of a reduced amount of plasma fibronectin on thrombus formation at arterial shear rate, we used the ferric chloride model of arterial injury in fibronectin heterozygote mice which have 50% of the normal plasma level of FN. Two groups of mice were observed by intravital microscopy - FN heterozygote (FN+/−) and corresponding age matched wild-type controls (FN +/+). The reduced level of pFN did not affect the early platelet interaction with subendothelium but caused a delay of several minutes in appearance of the first thrombus in the injured arteriole (15 min in FN +/− vs 6 min in FN+/+, p |
| Databáze: | OpenAIRE |
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