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http://hdl.handle.net/10261/213043
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Campo DC | Valor | Lengua/Idioma |
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dc.contributor.author | Zemankova, L. | es_ES |
dc.contributor.author | Varejckova, Michala | es_ES |
dc.contributor.author | Dolezelova, Eva | es_ES |
dc.contributor.author | Fikrova, Petra | es_ES |
dc.contributor.author | Jezkova, Katerina | es_ES |
dc.contributor.author | Rathouska, Jana | es_ES |
dc.contributor.author | Červený, Lukáš | es_ES |
dc.contributor.author | Botella, Luisa María | es_ES |
dc.contributor.author | Bernabéu, Carmelo | es_ES |
dc.contributor.author | Nachtigal, Petr | es_ES |
dc.date.accessioned | 2020-06-02T12:57:18Z | - |
dc.date.available | 2020-06-02T12:57:18Z | - |
dc.date.issued | 2015-06 | - |
dc.identifier.citation | J Physiol Pharmacol 66(3) 403-13 (2015) | es_ES |
dc.identifier.issn | 08675910 | - |
dc.identifier.issn | 18991505 | - |
dc.identifier.uri | http://hdl.handle.net/10261/213043 | - |
dc.description | 11 p.-6 fig. | es_ES |
dc.description.abstract | Endoglin, 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.sponsorship | This 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.iso | eng | es_ES |
dc.publisher | Polish Physiological Society | es_ES |
dc.relation | info:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/SAF2013-42421-R | es_ES |
dc.rights | closedAccess | es_ES |
dc.subject | Endothelial cells | es_ES |
dc.subject | Atorvastatin | es_ES |
dc.subject | Endothelial nitric oxide synthase | es_ES |
dc.subject | Endoglin | es_ES |
dc.subject | Human umbilical vein endothelial cells | es_ES |
dc.subject | Small interfering RNA | es_ES |
dc.subject | Tumor necrosis factor-alpha | es_ES |
dc.subject | Transforming growth factor-beta | es_ES |
dc.subject | Reactive oxygen species | es_ES |
dc.title | Atorvastatin-induced endothelial nitric oxide synthase expression in endothelial cells is mediated by endoglin | es_ES |
dc.type | artículo | es_ES |
dc.description.peerreviewed | Peer reviewed | es_ES |
dc.relation.publisherversion | http://www.jpp.krakow.pl/journal/archive/06_15/articles/09_article.html | es_ES |
dc.contributor.funder | Charles University (Czech Republic) | es_ES |
dc.contributor.funder | Ministerio de Economía y Competitividad (España) | es_ES |
dc.contributor.funder | Centro de Investigación Biomédica en Red Enfermedades Raras (España) | es_ES |
dc.contributor.funder | Instituto de Salud Carlos III | es_ES |
dc.contributor.funder | European Commission | es_ES |
dc.relation.csic | Sí | es_ES |
oprm.item.hasRevision | no ko 0 false | * |
dc.identifier.funder | http://dx.doi.org/10.13039/501100000780 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100004587 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100003329 | es_ES |
dc.contributor.orcid | Varejckova, Michala [0000-0002-5370-3194] | es_ES |
dc.contributor.orcid | Dolezelova, Eva [0000-0002-1397-6016] | es_ES |
dc.contributor.orcid | Fikrova, Petra [0000-0003-0484-6049] | es_ES |
dc.contributor.orcid | Jezkova, Katerina [0000-0001-5497-2313] | es_ES |
dc.contributor.orcid | Rathouska, Jana [0000-0001-6363-9715] | es_ES |
dc.contributor.orcid | Červený, Lukáš [0000-0002-1313-306X] | es_ES |
dc.contributor.orcid | Botella, Luisa María [0000-0002-6310-2245] | es_ES |
dc.contributor.orcid | Bernabéu, Carmelo [0000-0002-1563-6162] | es_ES |
dc.contributor.orcid | Nachtigal, Petr [0000-0001-9568-7295] | es_ES |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.cerifentitytype | Publications | - |
item.languageiso639-1 | en | - |
item.grantfulltext | none | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | No Fulltext | - |
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