|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
3
|
|
pubmed:dateCreated |
2001-6-13
|
|
pubmed:abstractText |
Hyperhomocysteinemia 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.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Homocysteine,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Jun
|
|
pubmed:issn |
0360-3997
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
25
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
179-86
|
|
pubmed:dateRevised |
2008-11-21
|
|
pubmed:meshHeading |
pubmed-meshheading:11403209-Arteriosclerosis,
pubmed-meshheading:11403209-Cells, Cultured,
pubmed-meshheading:11403209-Chemokine CCL2,
pubmed-meshheading:11403209-Chemokines,
pubmed-meshheading:11403209-Cytokines,
pubmed-meshheading:11403209-Drug Synergism,
pubmed-meshheading:11403209-Homocysteine,
pubmed-meshheading:11403209-Humans,
pubmed-meshheading:11403209-Hyperhomocysteinemia,
pubmed-meshheading:11403209-Interferon-gamma,
pubmed-meshheading:11403209-Interleukin-1,
pubmed-meshheading:11403209-Interleukin-8,
pubmed-meshheading:11403209-Muscle, Smooth, Vascular,
pubmed-meshheading:11403209-NF-kappa B,
pubmed-meshheading:11403209-RNA, Messenger,
pubmed-meshheading:11403209-Risk Factors,
pubmed-meshheading:11403209-Transcription Factor AP-1,
pubmed-meshheading:11403209-Tumor Necrosis Factor-alpha,
pubmed-meshheading:11403209-Up-Regulation
|
|
pubmed:year |
2001
|
|
pubmed:articleTitle |
Homocysteine augments cytokine-induced chemokine expression in human vascular smooth muscle cells: implications for atherogenesis.
|
|
pubmed:affiliation |
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602, USA.
|
|
pubmed:publicationType |
Journal Article
|
