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dc.contributor.authorZemankova, L.es_ES
dc.contributor.authorVarejckova, Michalaes_ES
dc.contributor.authorDolezelova, Evaes_ES
dc.contributor.authorFikrova, Petraes_ES
dc.contributor.authorJezkova, Katerinaes_ES
dc.contributor.authorRathouska, Janaes_ES
dc.contributor.authorČervený, Lukášes_ES
dc.contributor.authorBotella, Luisa Maríaes_ES
dc.contributor.authorBernabéu, Carmeloes_ES
dc.contributor.authorNachtigal, Petres_ES
dc.date.accessioned2020-06-02T12:57:18Z-
dc.date.available2020-06-02T12:57:18Z-
dc.date.issued2015-06-
dc.identifier.citationJ Physiol Pharmacol 66(3) 403-13 (2015)es_ES
dc.identifier.issn08675910-
dc.identifier.issn18991505-
dc.identifier.urihttp://hdl.handle.net/10261/213043-
dc.description11 p.-6 fig.es_ES
dc.description.abstractEndoglin, a transforming growth factor β (TGF-β) receptor type III, is co-expressed with endothelial nitric oxide synthase (eNOS) in aortic endothelium in atherosclerotic plaques of mice. Interestingly, atorvastatin (ATV) is able to increase both endoglin and eNOS expression and reduce plaque size beyond its lipid lowering effects but by unknown mechanisms. We hypothesized whether inflammation modulates ATV-dependent induction of endoglin and eNOS expression in vitro in endothelial cells and whether ATV-induced eNOS expression is regulated via endoglin. After treatment of human umbilical vein endothelial cells (HUVECs) with TNF-α, endoglin and eNOS protein expression was reduced, concomitantly with increased levels of cell surface VCAM-1 and soluble endoglin, as determined by flow cytometry, Western blot and ELISA analyses. By contrast, ATV treatment increased endoglin and eNOS protein expression, while preventing TNF-α-mediated downregulation of endoglin and eNOS protein levels. Moreover, suppression of endoglin using small interfering RNA (siRNA), but not inhibition of TGF-β signaling with SB431542, abrogated ATV-induced eNOS expression. These results suggest that ATV treatment prevents inflammation-reduced endoglin and eNOS expression in endothelial cells and that ATV-induced eNOS expression strongly depends on the proper expression of endoglin in HUVECs. Possible implications of these findings might be reflected in pathological conditions characterized by reduced expression of endoglin and eNOS as for example in hereditary hemorrhagic telangiectasia or in other endothelial dysfunctions.es_ES
dc.description.sponsorshipThis work was supported by The Grant Agency of Charles University in Prague (300811/C and 1158413/C), Charles University in Prague (SVV/2014/260064), Ministerio de Economía y Competitividad of Spain Raras ( (SAF2010-19222 and SAF2013-42421-R to CB), and Centro de Investigación Biomédica en Red de Enfermedades CIBERER to CB).CIBERER is an initiative of the Instituto de Salud Carlos III (ISCIII) of Spain supported by FEDER funds. The publication is co-financed by the European Social Fund and the state budget of the Czech Republic (Project No. CZ.1.07/2.3.00/30.0061).es_ES
dc.language.isoenges_ES
dc.publisherPolish Physiological Societyes_ES
dc.relationinfo:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/SAF2013-42421-Res_ES
dc.rightsclosedAccesses_ES
dc.subjectEndothelial cellses_ES
dc.subjectAtorvastatines_ES
dc.subjectEndothelial nitric oxide synthasees_ES
dc.subjectEndoglines_ES
dc.subjectHuman umbilical vein endothelial cellses_ES
dc.subjectSmall interfering RNAes_ES
dc.subjectTumor necrosis factor-alphaes_ES
dc.subjectTransforming growth factor-betaes_ES
dc.subjectReactive oxygen specieses_ES
dc.titleAtorvastatin-induced endothelial nitric oxide synthase expression in endothelial cells is mediated by endoglines_ES
dc.typeartículoes_ES
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttp://www.jpp.krakow.pl/journal/archive/06_15/articles/09_article.htmles_ES
dc.contributor.funderCharles University (Czech Republic)es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderCentro de Investigación Biomédica en Red Enfermedades Raras (España)es_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.contributor.funderEuropean Commissiones_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.contributor.orcidVarejckova, Michala [0000-0002-5370-3194]es_ES
dc.contributor.orcidDolezelova, Eva [0000-0002-1397-6016]es_ES
dc.contributor.orcidFikrova, Petra [0000-0003-0484-6049]es_ES
dc.contributor.orcidJezkova, Katerina [0000-0001-5497-2313]es_ES
dc.contributor.orcidRathouska, Jana [0000-0001-6363-9715]es_ES
dc.contributor.orcidČervený, Lukáš [0000-0002-1313-306X]es_ES
dc.contributor.orcidBotella, Luisa María [0000-0002-6310-2245]es_ES
dc.contributor.orcidBernabéu, Carmelo [0000-0002-1563-6162]es_ES
dc.contributor.orcidNachtigal, Petr [0000-0001-9568-7295]es_ES
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairetypeartículo-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
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