EMILIN2 (Elastin microfibril interface located protein), potential modifier of thrombosis
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ORIGINAL BASIC RESEARCH
Open Access
EMILIN2 (Elastin microfibril interface located protein), potential modifier of thrombosis Qila Sa and Jane L Hoover-Plow*
Abstract Background: Elastin microfibril interface located protein 2 (EMILIN2) is an extracellular glycoprotein associated with cardiovascular development. While other EMILIN proteins are reported to play a role in elastogenesis and coagulation, little is known about EMILIN2 function in the cardiovascular system. The objective of this study was to determine whether EMILIN2 could play a role in thrombosis. Results: 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. Conclusions: These results suggest EMILIN2 could play a role in thrombosis as a constituent of the vessel wall and/or a component of the thrombus.
Background 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 * Correspondence: [email protected] Joseph J. Jacobs Center For Thrombosis and Vascular Biology, Department of Cardiovascular Medicine and Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
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 of thrombosis in the last decade. However, strategies to prevent thrombosis have lagged far behind, due in part to the contribution of multiple and as yet undefined genetic factors that lead to thrombotic risk. The obje
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