Source:http://linkedlifedata.com/resource/pubmed/id/18787184
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
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| pubmed:dateCreated |
2008-10-23
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| pubmed:abstractText |
Background- Vascular cell adhesion molecule-1 (VCAM-1) is critical in monocyte recruitment to the endothelium, a key event in development of atherosclerotic lesions. Stimulation of human coronary artery endothelial cells (HCAECs) with ATP positively modulates VCAM-1 expression and function through a mechanism involving Ca(2+) signaling. We here examined the role of Ca(2+) influx and native TRPC3 channels in that mechanism. METHODS AND RESULTS: Omission of extracellular Ca(2+) or pretreatment of cells with channel blockers markedly reduced ATP-induced VCAM-1 and monocyte adhesion. Using a siRNA strategy and real-time fluorescence, we found that native TRPC3 proteins contribute to constitutive and ATP-regulated Ca(2+) influx. ATP-dependent upregulation of VCAM-1 was accompanied by an increase in basal cation entry and TRPC3 expression. Notably, TRPC3 knock-down resulted in a dramatic reduction of ATP-induced VCAM-1 and monocyte adhesion. CONCLUSIONS: These findings indicate that in HCAECs, native TRPC3 proteins form channels that contribute to constitutive and ATP-dependent Ca(2+) influx, and that TRPC3 expression and function are fundamental to support VCAM-1 expression and monocyte binding. This is the first evidence to date relating native TRPC3 proteins with regulated expression of cell adhesion molecules in coronary endothelium, and suggests a potential pathophysiological role of TRPC3 in coronary artery disease.
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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/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/TRPC Cation Channels,
http://linkedlifedata.com/resource/pubmed/chemical/TRPC3 cation channel,
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 |
Nov
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| pubmed:issn |
1524-4636
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
28
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2049-55
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| pubmed:meshHeading |
pubmed-meshheading:18787184-Adenosine Triphosphate,
pubmed-meshheading:18787184-Calcium Channel Blockers,
pubmed-meshheading:18787184-Calcium Signaling,
pubmed-meshheading:18787184-Cell Adhesion,
pubmed-meshheading:18787184-Cells, Cultured,
pubmed-meshheading:18787184-Coronary Artery Disease,
pubmed-meshheading:18787184-Coronary Vessels,
pubmed-meshheading:18787184-Endothelial Cells,
pubmed-meshheading:18787184-Humans,
pubmed-meshheading:18787184-Monocytes,
pubmed-meshheading:18787184-RNA, Small Interfering,
pubmed-meshheading:18787184-RNA Interference,
pubmed-meshheading:18787184-TRPC Cation Channels,
pubmed-meshheading:18787184-Time Factors,
pubmed-meshheading:18787184-Tumor Necrosis Factor-alpha,
pubmed-meshheading:18787184-U937 Cells,
pubmed-meshheading:18787184-Up-Regulation,
pubmed-meshheading:18787184-Vascular Cell Adhesion Molecule-1
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| pubmed:year |
2008
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| pubmed:articleTitle |
Involvement of native TRPC3 proteins in ATP-dependent expression of VCAM-1 and monocyte adherence in coronary artery endothelial cells.
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| pubmed:affiliation |
Department of Physiology and Pharmacology, Center for Diabetes and Endocrine Research, University of Toledo College of Medicine, Health Science Campus, Ohio 43614, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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