| pubmed-article:19193866 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19193866 | lifeskim:mentions | umls-concept:C0079281 | lld:lifeskim |
| pubmed-article:19193866 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:19193866 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:19193866 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19193866 | pubmed:dateCreated | 2009-4-1 | lld:pubmed |
| pubmed-article:19193866 | pubmed:abstractText | We previously demonstrated that fibrinogen (Fg) binding to the vascular endothelial intercellular adhesion molecule-1 (ICAM-1) leads to microvascular constriction in vivo and in vitro. Although a role of endothelin-1 (ET-1) in this Fg-induced vasoconstriction was suggested, the mechanism of action was not clear. In the current study, we tested the hypothesis that Fg-induced vasoconstriction results from ET-1 production by vascular endothelial cells (EC) and is mediated by activation of extracellular signal-regulated kinase -1/2 (ERK-1/2). Confluent, rat heart microvascular endothelial cells (RHMECs) were treated with one of the following: Fg (2 or 4 mg/ml), Fg (4 mg/ml) with ERK-1/2 kinase inhibitors (PD-98059 or U-0126), Fg (4 mg/ml) with an antibody against ICAM-1, or medium alone for 45 min. The amount of ET-1 formed and the concentration of released von Willebrand factor (vWF) in the cell culture medium were measured by ELISAs. Fg-induced exocytosis of Weibel-Palade bodies (WPBs) was assessed by immunocytochemistry. Phosphorylation of ERK-1/2 was detected by Western blot analysis. Fg caused a dose-dependent increase in ET-1 formation and release of vWF from the RHMECs. This Fg-induced increase in ET-1 production was inhibited by specific ERK-1/2 kinase inhibitors and by anti-ICAM-1 antibody. Immunocytochemical staining showed that an increase in Fg concentration enhanced exocytosis of WPBs in ECs. A specific endothelin type B receptor blocker, BQ-788, attenuated the enhanced phosphorylation of ERK-1/2 in ECs caused by increased Fg content in the culture medium. The presence of an endothelin converting enzyme inhibitor, SM-19712, slightly decreased Fg-induced phosphorylation of ERK-1/2, but inhibited production of Fg-induced ET-1 production. These results suggest that Fg-induced vasoconstriction may be mediated, in part, by activation of ERK-1/2 signaling and increased production of ET-1 that further increases EC ERK-1/2 signaling. Thus, an increased content of Fg may enhance vasoconstriction through increased production of ET-1. | lld:pubmed |
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| pubmed-article:19193866 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19193866 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19193866 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19193866 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:19193866 | pubmed:issn | 0363-6143 | lld:pubmed |
| pubmed-article:19193866 | pubmed:author | pubmed-author:RobertsAndrew... | lld:pubmed |
| pubmed-article:19193866 | pubmed:author | pubmed-author:TyagiSuresh... | lld:pubmed |
| pubmed-article:19193866 | pubmed:author | pubmed-author:LominadzeDavi... | lld:pubmed |
| pubmed-article:19193866 | pubmed:author | pubmed-author:DeanWilliam... | lld:pubmed |
| pubmed-article:19193866 | pubmed:author | pubmed-author:SenUtpalU | lld:pubmed |
| pubmed-article:19193866 | pubmed:author | pubmed-author:TyagiNeetuN | lld:pubmed |
| pubmed-article:19193866 | pubmed:author | pubmed-author:PatibandlaPha... | lld:pubmed |
| pubmed-article:19193866 | pubmed:issnType | Print | lld:pubmed |
