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dc.contributor.author | Glineur, Corine | - |
dc.contributor.author | Gross, Barbara | - |
dc.contributor.author | Neve, Bernadette | - |
dc.contributor.author | Rommens, Corinne | - |
dc.contributor.author | Chew, Gerard T. | - |
dc.contributor.author | Marin-Nizard, Françoise | - |
dc.contributor.author | Rodríguez-Pascual, Fernando | - |
dc.contributor.author | Lamas Peláez, Santiago | - |
dc.contributor.author | Watts, Gerard F. | - |
dc.contributor.author | Staels, Bart | - |
dc.date.accessioned | 2014-04-25T11:06:18Z | - |
dc.date.available | 2014-04-25T11:06:18Z | - |
dc.date.issued | 2013 | - |
dc.identifier | doi: 10.1161/ATVBAHA.112.300665 | - |
dc.identifier | issn: 1079-5642 | - |
dc.identifier.citation | Arteriosclerosis, Thrombosis, and Vascular Biology 33: 621- 628 (2013) | - |
dc.identifier.uri | http://hdl.handle.net/10261/95891 | - |
dc.description.abstract | Objective-Dyslipidemia contributes to endothelial dysfunction in type 2 diabetes mellitus. Fenofibrate (FF), a ligand of the peroxisome proliferator-activated receptor-α (PPARα), has beneficial effects on microvascular complications. FF may act on the endothelium by regulating vasoactive factors, including endothelin-1 (ET-1). In vitro, FF decreases ET-1 expression in human microvascular endothelial cells. We investigated the molecular mechanisms involved in the effect of FF treatment on plasma levels of ET-1 in type 2 diabetes mellitus patients. Methods and Results-FF impaired the capacity of transforming growth factor-β to induce ET-1 gene expression. PPARα activation by FF increased expression of the transcriptional repressor Krüppel-like factor 11 and its binding to the ET-1 gene promoter. Knockdown of Krüppel-like factor 11 expression potentiated basal and transforming growth factor-β-stimulated ET-1 expression, suggesting that Krüppel-like factor 11 downregulates ET-1 expression. FF, in a PPARα-independent manner, and insulin enhanced glycogen synthase kinase-3β phosphorylation thus reducing glycogen synthase kinase-3 activity that contributes to the FF-mediated reduction of ET-1 gene expression. In type 2 diabetes mellitus, improvement of flow-mediated dilatation of the brachial artery by FF was associated with a decrease in plasma ET-1. Conclusion-FF decreases ET-1 expression by a PPARα-dependent mechanism, via transcriptional induction of the Krüppel-like factor 11 repressor and by PPARα-independent actions via inhibition of glycogen synthase kinase-3 activity. © 2013 American Heart Association, Inc. | - |
dc.description.sponsorship | Région Nord-Pas de Calais/FEDER; Fondation Coeur et Artères; National Health and Medical Research Council (NHMRC) of Australia; NHMRC medical scholarship; French National Research Agency (ANR) Institut National de la Santé et de la Recherche Médicale; Centre National de la Recherche Scientifique; Institut Universitaire de France | - |
dc.publisher | American Heart Association | - |
dc.rights | openAccess | - |
dc.subject | Endothelium | - |
dc.subject | Glycogen synthase kinase-3 | - |
dc.subject | Peroxisome proliferator–activated receptor-α | - |
dc.subject | Type 2 diabetes mellitus | - |
dc.subject | Endothelin-1 | - |
dc.title | Fenofibrate inhibits endothelin-1 expression by peroxisome proliferator-activated receptor α-dependent and independent mechanisms in human endothelial cells | - |
dc.type | artículo | - |
dc.identifier.doi | 10.1161/ATVBAHA.112.300665 | - |
dc.date.updated | 2014-04-25T11:06:18Z | - |
dc.description.version | Peer Reviewed | - |
dc.language.rfc3066 | eng | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.grantfulltext | open | - |
item.cerifentitytype | Publications | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | With Fulltext | - |
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S_Lamas_Arte_Throm_Vas_Biol.pdf | 1,5 MB | Adobe PDF | Visualizar/Abrir |
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