Source:http://linkedlifedata.com/resource/pubmed/id/10430178
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rdf:type | |
lifeskim:mentions |
umls-concept:C0003483,
umls-concept:C0017262,
umls-concept:C0021758,
umls-concept:C0078056,
umls-concept:C0079904,
umls-concept:C0086418,
umls-concept:C0185117,
umls-concept:C0205217,
umls-concept:C0205263,
umls-concept:C0332281,
umls-concept:C0441889,
umls-concept:C0521447,
umls-concept:C1135918,
umls-concept:C2911684
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pubmed:issue |
3
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pubmed:dateCreated |
1999-8-16
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pubmed:abstractText |
Vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) are upregulated in vascular endothelial and smooth muscle cells by cytokines produced at sites of inflammation. The cytokine profile for induction of VCAM-1, however, is different for the two cell types. Tumor necrosis factor-alpha (TNF-alpha) induced both VCAM-1 and ICAM-1 expression in human umbilical vein endothelial cells (HUVECs; ED50 approximately 300 and 30 U/ml, respectively). TNF-alpha and interleukin-1beta (IL-1beta) stimulated cell surface ICAM-1 expression, but not VCAM-1 expression, in human aortic smooth muscle cells (HASMCs). Conversely, IL-4 was a potent VCAM-1 inducer in HASMCs (ED50 approximately 100 pg/ml) but did not induce ICAM-1 expression. Nuclear extracts from IL-4-treated cells were compared with untreated cells for relative nuclear factor-kappa B (NF-kappaB) levels by using an electrophoretic mobility shift assay and surface plasmon resonance techniques. No significant increase in nuclear NF-kappaB DNA binding activity was detected in IL-4-treated HASMCs by either method of analysis. IL-1beta and TNF-alpha stimulated nuclear NF-kappaB levels by about fourfold and fivefold, respectively, in HASMCs. The antioxidant pyrrolidine dithiocarbamate (PDTC) similarly inhibited VCAM-1 upregulation in HASMCs incubated with IL-4 and in HUVECs incubated with TNF-alpha (IC50s of 25 and 40 microM, respectively). These data suggest that a significant increase in nuclear NF-kappaB levels is not necessary or sufficient for VCAM-1 upregulation in HASMCs and does not determine the relative sensitivity to inhibition of gene expression by PDTC.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0021-9541
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
180
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
381-9
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:10430178-Aorta,
pubmed-meshheading:10430178-Cell Membrane,
pubmed-meshheading:10430178-Cells, Cultured,
pubmed-meshheading:10430178-Humans,
pubmed-meshheading:10430178-Interleukin-1,
pubmed-meshheading:10430178-Interleukin-4,
pubmed-meshheading:10430178-Muscle, Smooth, Vascular,
pubmed-meshheading:10430178-NF-kappa B,
pubmed-meshheading:10430178-Tumor Necrosis Factor-alpha,
pubmed-meshheading:10430178-Umbilical Veins,
pubmed-meshheading:10430178-Vascular Cell Adhesion Molecule-1
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pubmed:year |
1999
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pubmed:articleTitle |
Induction of vascular cell adhesion molecule-1 expression by IL-4 in human aortic smooth muscle cells is not associated with increased nuclear NF-kappaB levels.
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pubmed:affiliation |
Hoechst Marion Roussel, Inc., Bridgewater, New Jersey 08807-0800, USA. paul.wright@hmrag.com
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pubmed:publicationType |
Journal Article
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