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pubmed-article:11403209pubmed:abstractTextHyperhomocysteinemia is an independent risk factor for atherosclerosis and atherothrombosis. While in vitro studies have revealed a number of homocysteine-mediated alterations in the thromboregulatory properties of endothelial cells, comparatively little is known about homocysteine-modulated smooth muscle cell function. We observed that exposure of human aortic smooth muscle cells to pathophysiologically relevant concentrations of homocysteine results in concentration-dependent increases in cytokine-induced MCP-1 and IL-8 secretion. RNase protection assays revealed that both MCP-1 and IL-8 mRNA concentrations are increased in homocysteine-treated smooth muscle cells when compared to cells activated with cytokines alone. Homocysteine treatment also increased cytosolic-to-nuclear translocation of the p65 and p50 subunits of the Rel/NF-kappaB family of transcription factors but had no effect on AP-1 activation. Cumulatively, these data suggest that homocysteine may increase monocyte recruitment into developing atherosclerotic lesions by upregulating MCP-1 and IL-8 expression in vascular smooth muscle cells.lld:pubmed
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pubmed-article:11403209pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:11403209pubmed:articleTitleHomocysteine augments cytokine-induced chemokine expression in human vascular smooth muscle cells: implications for atherogenesis.lld:pubmed
pubmed-article:11403209pubmed:affiliationDepartment of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602, USA.lld:pubmed
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