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dc.contributor.authorVillalobos, Laura A.
dc.contributor.authorSan Hipólito-Luengo, Álvaro
dc.contributor.authorRamos-González, Mariella
dc.contributor.authorCercas, Elena
dc.contributor.authorVallejo, Susana
dc.contributor.authorRomero, Alejandra
dc.contributor.authorRomacho, Tania
dc.contributor.authorCarraro, Raffaele 
dc.contributor.otherUAM. Departamento de Farmacologíaes_ES
dc.contributor.otherUAM. Departamento de Medicinaes_ES
dc.contributor.otherInstituto de Investigación del Hospital de La Princesa (IP)es_ES
dc.date.accessioned2017-04-25T10:44:52Z
dc.date.available2017-04-25T10:44:52Z
dc.date.issued2016-01-01
dc.identifier.citationFrontiers in Pharmacology 7 (2016): Article 482en_US
dc.identifier.issn1663-9812es_ES
dc.identifier.urihttp://hdl.handle.net/10486/678014
dc.description.abstractBackground and Aims: Targeting inflammation is nowadays considered as a challenging pharmacological strategy to prevent or delay the development of vascular diseases. Angiotensin-(1-7) is a member of the renin-angiotensin system (RAS) that binds Mas receptors and has gained growing attention in the last years as a regulator of vascular homeostasis. Here, we explored the capacity of Ang-(1-7) to counteract human aortic smooth muscle cell (HASMC) inflammation triggered by RAS-dependent and -independent stimuli, such as Ang II or interleukin (IL)-1β. Methods and Results: In cultured HASMC, the expression of inducible nitric oxide synthase (iNOS) and the release of nitric oxide were stimulated by both Ang II and IL-1β, as determined by Western blot and indirect immunofluorescence or the Griess method, respectively. iNOS induction was inhibited by Ang-(1-7) in a concentration-dependent manner. This effect was equally blocked by two different Mas receptor antagonists, A779 and D-Pro7-Ang-(1-7), suggesting the participation of a unique Mas receptor subtype. Using pharmacological inhibitors, the induction of iNOS was proven to rely on the consecutive upstream activation of NADPH oxidase and nuclear factor (NF)-κB. Indeed, Ang-(1-7) markedly inhibited the activation of the NADPH oxidase and subsequently of NF-κB, as determined by lucigenin-derived chemiluminescence and electromobility shift assay, respectively. Conclusion: Ang-(1-7) can act as a counter-regulator of the inflammation of vascular smooth muscle cells triggered by Ang II, but also by other stimuli beyond the RAS. Activating or mimicking the Ang-(1-7)/Mas axis may represent a pharmacological opportunity to attenuate the pro-inflammatory environment that promotes and sustains the development of vascular diseases.en_US
dc.description.sponsorshipThis work was funded by grants from Ministerio de Economía y Competitividad (SAF2014-52762-R)en_US
dc.format.extent10 pag.es_ES
dc.format.mimetypeapplication/pdfen
dc.language.isoengen
dc.publisherFrontiers Mediaen_US
dc.relation.ispartofFrontiers in Pharmacologyen_US
dc.rights© 2016 Villalobos, San Hipólito-Luengo, Ramos-González, Cercas, Vallejo, Romero, Romacho, Carraro, Sánchez-Ferrer and Peiró.es_ES
dc.subject.otherAngiotensin-(1-7)en_US
dc.subject.otherCell signalingen_US
dc.subject.otherCytokinesen_US
dc.subject.otherInducible nitric oxide synthaseen_US
dc.subject.otherInflammationen_US
dc.subject.otherInterleukin-1βen_US
dc.subject.otherMas receptorsen_US
dc.subject.otherVascular smooth muscleen_US
dc.titleThe angiotensin-(1-7)/mas axis counteracts angiotensin II-dependent and -independent pro-inflammatory signaling in human vascular smooth muscle cellsen_US
dc.typearticleen
dc.subject.ecienciaMedicinaes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.3389/fphar.2016.00482es_ES
dc.identifier.doi10.3389/fphar.2016.00482es_ES
dc.identifier.publicationfirstpage482-1es_ES
dc.identifier.publicationlastpage482-10es_ES
dc.identifier.publicationvolume7es_ES
dc.relation.projectIDGobierno de España. SAF2014-52762-Res_ES
dc.type.versioninfo:eu-repo/semantics/publishedVersionen
dc.rights.ccReconocimientoes_ES
dc.rights.accessRightsopenAccessen
dc.authorUAMSan Hipólito Luengo, Álvaro (278899)
dc.facultadUAMFacultad de Medicina
dc.institutoUAMInstituto de Investigación Sanitaria Hospital Universitario de La Paz (IdiPAZ)


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