Source:http://linkedlifedata.com/resource/pubmed/id/16603696
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2006-8-10
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pubmed:abstractText |
Monocyte-endothelial cell adhesion is a key early event in atherogenesis. C-reactive protein (CRP), a cardiovascular risk marker, is known to stimulate ICAM and VCAM in human aortic endothelial cells (HAEC) and induces monocyte-endothelial cell adhesion. In this study, we examined the mechanisms by which native CRP promotes monocyte-endothelial cell adhesion under static conditions and tested the effect of CRP on adhesion under shear flow. Incubation of HAEC with CRP (>25 microg/ml) upregulated NF-kappaB activity, and this resulted in a significant increase in ICAM (54% increase, P<0.001), VCAM (41% increase, P<0.01), and monocyte-endothelial cell adhesion (44% increase, P<0.02) compared with those of control. Preincubation with antibodies to CD32 and CD64 but not CD16 effectively inhibited this activation. Blocking NF-kappaB activity with inhibitors or a dominant negative inhibitory kappaB significantly decreased ICAM, VCAM upregulation, and subsequent monocyte-endothelial cell adhesion. Preincubation with antibodies to CD32 and CD64 or transient transfection with small interference RNA to CD32 attenuated CRP-induced NF-kappaB activity, ICAM, VCAM, and monocyte-endothelial cell adhesion under static conditions. Also, the Syk kinase inhibitor piceatannol and MG-132, a proteasome degradation inhibitor, produced similar attenuation in NF-kappaB activity, ICAM, VCAM, and adhesion. Furthermore, CRP-activated endothelial cells supported monocyte rolling, arrest, and transmigration in shear flow (2 dyn/cm2), and this was also inhibited by preincubation with antibodies to CD32 and CD64. Thus, in HAEC, CRP upregulates monocyte-endothelial adhesion by activation of NF-kappaB through engaging the Fcgamma receptors CD32 and CD64.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/C-Reactive Protein,
http://linkedlifedata.com/resource/pubmed/chemical/E-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgG,
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 |
0363-6135
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
291
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H1170-6
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:16603696-Antibodies,
pubmed-meshheading:16603696-Aorta,
pubmed-meshheading:16603696-C-Reactive Protein,
pubmed-meshheading:16603696-Cell Adhesion,
pubmed-meshheading:16603696-E-Selectin,
pubmed-meshheading:16603696-Endothelium, Vascular,
pubmed-meshheading:16603696-Humans,
pubmed-meshheading:16603696-Intercellular Adhesion Molecule-1,
pubmed-meshheading:16603696-Monocytes,
pubmed-meshheading:16603696-NF-kappa B,
pubmed-meshheading:16603696-RNA, Small Interfering,
pubmed-meshheading:16603696-Receptors, IgG,
pubmed-meshheading:16603696-Up-Regulation,
pubmed-meshheading:16603696-Vascular Cell Adhesion Molecule-1
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pubmed:year |
2006
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pubmed:articleTitle |
CRP promotes monocyte-endothelial cell adhesion via Fcgamma receptors in human aortic endothelial cells under static and shear flow conditions.
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pubmed:affiliation |
Laboratory for Atherosclerosis and Metabolic Research, 4635 II Ave., Res. 1 Bldg., Rm. 3000, University of California Davis Medical Center, Sacramento, CA 95817, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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