Glycosaminoglycans as Key Molecules in Atherosclerosis: The Role of Versican and Hyaluronan
Abstract:Cardiovascular disease is the largest cause of death in Western societies and it primarily results from atherosclerosis of large and medium-sized vessels. Atherosclerosis leads to myocardial infarction, when it occurs in the coronary arteries, or stroke, when it occurs in the cerebral arteries. Pathological processes involved in macrovascular disease include the accumulation of lipids which are retained by extracellular matrix (ECM) molecules, especially by the chondroitin sulfate/dermatan sulfate (CS/DS) proteoglycans (CS/DSPGs), such as versican, biglycan and decorin. The sulfation pattern of CS is a key player in protein interactions causing atherosclerosis. Several studies have shown that lipoproteins bind CSPGs via their glycosaminoglycan chains. Galactosaminoglycans, such as CS and DS, bind low density lipoproteins (LDL), affecting the role of these molecules in the arterial wall. In this article, the role of CS and versican in atherosclerosis and hyaluronan in atherogenesis as well as the up to date known mechanisms that provoke this pathological condition are presented and discussed.
Keywords: ADAMTS; AoSMCs; Atherosclerosis; CS/DS; CS/DSPGs; Dglucuronic acid; GAGs; GalAGs; Galactosaminoglycans; Glycosaminoglycans; HARE; Hyaluronan; Hyaluronan Receptor for Endocytosis; Hyaluronan-Mediated Motility; LYVE-1; Lymphatic Vessel Endothelial Receptor 1; N-acetyl-D-galactosamine; RHAMM; TFPI-1; TLR4; Tissue Factor Pathway Inhibitor-1; Toll Like Receptors 4; VCAM-1; cellular mechanisms; chondroitin sulfate; chondroitin sulfate/dermatan sulfate; glycosaminoglycans; human aortic smooth muscle cells; lipoproteins; proteoglycans; vascular cell adhesion molecule-1; versican
Document Type: Research Article
Publication date: January 1, 2010
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