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EMILIN2 (Elastin microfibril interface located protein), potential modifier of thrombosis

DOI: 10.1186/1477-9560-9-9

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Abstract:

EMILIN2 mRNA was expressed in 8 wk old C57BL/6J mice in lung, heart, aorta and bone marrow, with the highest expression in bone marrow. In mouse cells, EMILIN2 mRNA expression in macrophages was higher than expression in endothelial cells and fibroblasts. EMILIN2 was identified with cells and extracellular matrix by immunohistochemistry in the carotid and aorta. After carotid ferric chloride injury, EMILIN2 was abundantly expressed in the thrombus and inhibition of EMILIN2 increased platelet de-aggregation after ADP-stimulated platelet aggregation.These results suggest EMILIN2 could play a role in thrombosis as a constituent of the vessel wall and/or a component of the thrombus.The clinical manifestations of arterial and venous thrombosis represent the leading causes of death in the developed world [1]. While arterial and venous thrombosis have fundamental pathobiological differences, both are complex [2] and are influenced by multiple genetic and environmental factors [3]. Acute thrombosis at the site of a plaque is thought to be a precipitating event in the transition from a stable or subclinical atherosclerotic disease to acute myocardial infarction, ischemic stroke or peripheral arterial occlusion. For individuals undergoing surgery, thromboembolism and venous thrombosis are common. Twin and sibling studies [4] show that inherited risk factors contribute significantly to the development of coronary artery disease and ischemic stroke. Genetic abnormalities that influence production, activity, or metabolism can shift the balance in favor of thrombosis. Polymorphisms [2,5] in coagulation factors, fibrinolytic factors, platelet surface receptors, methylenetetrahydrofolate reductase, endothelial nitric oxide synthase and antioxidant enzymes have been implicated as genetic factors of risk for thrombosis. The role of many of these risk factors in thrombotic diseases has been replicated in animal models [6-11]. Great strides have been made in the diagnosis and treatment

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