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

Qila Sa,Jane L Hoover-Plow

doi:10.1186/1477-9560-9-9

Abstract

BackgroundElastin 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.ResultsEMILIN2 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.ConclusionsThese results suggest EMILIN2 could play a role in thrombosis as a constituent of the vessel wall and/or a component of the thrombus.

Highlights

Elastin microfibril interface located protein 2 (EMILIN2) is an extracellular glycoprotein associated with cardiovascular development
Distribution of Emilin2 mRNA in tissues The mRNA expression of Emilin2 was determined by quantitative real-time PCR in lung, heart, aorta and bone marrow cells (Figure 2A)
The expression in the bone marrow was 20-fold higher than in the lung. This suggests that bone marrow is a major source of Emilin2 and is unlike Emilin1 expression [21] where the major source is the vessel wall

Summary

Introduction

Elastin microfibril interface located protein 2 (EMILIN2) is an extracellular glycoprotein associated with cardiovascular development. The objective of this study was to determine whether EMILIN2 could play a role in thrombosis. While arterial and venous thrombosis have fundamental pathobiological differences, both are complex [2] and are influenced by multiple genetic and environmental factors [3]. Twin and sibling studies [4] show that inherited risk factors contribute significantly to the development of coronary artery disease and ischemic stroke. 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 objective of this study was to investigate whether EMILIN2 (elastin microfibril interface located protein 2), distributed in the cardiovascular system during development [12], plays a role in thrombosis

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