dc.contributor.author | Alique, Matilde | |
dc.contributor.author | Sánchez-López, Elsa | |
dc.contributor.author | Rayego-Mateos, Sandra | |
dc.contributor.author | Egido, Jesús | |
dc.contributor.author | Ortiz Arduán, Alberto | |
dc.contributor.author | Ruiz Ortega, Marta | |
dc.contributor.other | UAM. Departamento de Medicina | es_ES |
dc.contributor.other | Instituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD) | es_ES |
dc.date.accessioned | 2016-06-10T14:47:59Z | |
dc.date.available | 2016-06-10T14:47:59Z | |
dc.date.issued | 2015-01-01 | |
dc.identifier.citation | JRAAS - Journal of the Renin-Angiotensin-Aldosterone System 16.1 (2015): 23-32 | es_ES |
dc.identifier.issn | 1470-3203 | es_ES |
dc.identifier.issn | 1752-8976 (on line) | es_ES |
dc.identifier.uri | http://hdl.handle.net/10486/671386 | |
dc.description.abstract | Introduction: The nuclear factor-κB (NF-κB) is an important regulator of the inflammatory response. Angiotensin II
(Ang II) activates the NF-κB pathway linked to renal inflammation. Although both AT1 and AT2 receptors are involved
in Ang II-mediated NF-κB activation, the biological processes mediated by each receptor are not fully characterized.
Interleukin-1β (IL-1β) is an important macrophage-derived cytokine that regulates immune and inflammatory processes,
activating intracellular pathways shared with Ang II, including the NF-κB.
Materials and methods: In vitro studies were done in primary cultured rat mesangial cells. NF-κB pathway was
evaluated by phosphorylated levels of p65/IκB and DNA binding activity. The Ang II receptor subtype was determined
by pretreatment with AT1 and AT2 antagonists.
Results: In mesangial cells the simultaneous presence of Ang II and IL-1β caused a synergistic activation of the NF-κB
pathway and a marked upregulation of proinflammatory factors under NF-κB control, including monocyte chemoattractant
protein-1. The AT1, but not AT2, antagonist abolished the synergistic effect on NF-κB activation and proinflammatory
genes caused by coincubation of Ang II and IL-1β.
Conclusions: These data indicates that Ang II, via AT1/NF-κB pathway activation, cooperates with IL-β to increase the
inflammatory response in mesangial cells | es_ES |
dc.description.sponsorship | This work was supported by grants from the Instituto de Salud
Carlos III (ISCIIIRETIC REDinREN RD06/0016, RD12/0021,
PI11/01854), Comunidad de Madrid (Fibroteam S2010/BMD-
2321, S2010/BMD-2378), and Research Institute Queen Sophia
(IRSIN). Programa Intensificación Actividad Investigadora
(ISCIII/Agencia Laín-Entralgo/CM) to AO. MA and ESL are supported
by a ‘Sara Borrell’ postdoctoral contract from Instituto de
Salud Carlos III (CD10/00347 and CD09/00066, respectively) | es_ES |
dc.format.extent | 10 pag. | es_ES |
dc.format.mimetype | application/pdf | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | SAGE Publications | es_ES |
dc.relation.ispartof | JRAAS - Journal of the Renin-Angiotensin-Aldosterone System | es_ES |
dc.rights | © The Author(s) 2014 | es_ES |
dc.subject.other | Angiotensin II | es_ES |
dc.subject.other | Cytokines | es_ES |
dc.subject.other | Mesangial cells | es_ES |
dc.subject.other | Transcription factors | es_ES |
dc.subject.other | Kinases | es_ES |
dc.subject.other | Chemokine | es_ES |
dc.title | Angiotensin II, via angiotensin receptor type 1/nuclear factor-κB activation, causes a synergistic effect on interleukin-1-β-induced inflammatory responses in cultured mesangial cells | es_ES |
dc.type | article | es_ES |
dc.subject.eciencia | Medicina | es_ES |
dc.relation.publisherversion | http://dx.doi.org/10.1177/1470320314551564 | es_ES |
dc.identifier.doi | 10.1177/1470320314551564 | es_ES |
dc.identifier.publicationfirstpage | 23 | es_ES |
dc.identifier.publicationissue | 1 | es_ES |
dc.identifier.publicationlastpage | 32 | es_ES |
dc.identifier.publicationvolume | 16 | es_ES |
dc.relation.projectID | Comunidad de Madrid. S2010/BMD- 2321/FIBROTEAM | es_ES |
dc.relation.projectID | Comunidad de Madrid. S2010/BMD-2378/CIFRA | es_ES |
dc.type.version | info:eu-repo/semantics/publishedVersion | es_ES |
dc.rights.cc | Reconocimiento – NoComercial | es_ES |
dc.rights.accessRights | openAccess | es_ES |
dc.facultadUAM | Facultad de Medicina | |
dc.institutoUAM | Instituto de Investigación Sanitaria Fundación Jiménez Díaz (ISS-FJD) | |