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http://hdl.handle.net/10261/130266
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dc.contributor.author | Rodríguez-Peña, Ana B. | - |
dc.contributor.author | Fuentes-Calvo, Isabel | - |
dc.contributor.author | Docherty, Neil G. | - |
dc.contributor.author | Arévalo, Miguel | - |
dc.contributor.author | Grande, M. Teresa | - |
dc.contributor.author | Eleno, Nélida | - |
dc.contributor.author | Pérez-Barriocanal, Fernando | - |
dc.contributor.author | López-Novoa, José M. | - |
dc.date.accessioned | 2016-03-18T12:18:26Z | - |
dc.date.available | 2016-03-18T12:18:26Z | - |
dc.date.issued | 2014 | - |
dc.identifier | doi: 10.1155/2014/124902 | - |
dc.identifier | issn: 2314-6133 | - |
dc.identifier | e-issn: 2314-6141 | - |
dc.identifier.citation | BioMed Research International: 124902 (2014) | - |
dc.identifier.uri | http://hdl.handle.net/10261/130266 | - |
dc.description | This is an open access article distributed under the Creative Commons Attribution License. | - |
dc.description.abstract | Tubulointerstitial fibrosis is a major feature of chronic kidney disease. Unilateral ureteral obstruction (UUO) in rodents leads to the development of renal tubulointerstitial fibrosis consistent with histopathological changes observed in advanced chronic kidney disease in humans. The purpose of this study was to assess the effect of inhibiting angiotensin II receptors or Ras activation on early renal fibrotic changes induced by UUO. Animals either received angiotensin II or underwent UUO. UUO animals received either losartan, atorvastatin, and farnesyl transferase inhibitor (FTI) L-744,832, or chaetomellic acid A (ChA). Levels of activated Ras, phospho-ERK1/2, phospho-Akt, fibronectin, and α-smooth muscle actin were subsequently quantified in renal tissue by ELISA, Western blot, and/or immunohistochemistry. Our results demonstrate that administration of angiotensin II induces activation of the small GTPase Ras/Erk/Akt signaling system, suggesting an involvement of angiotensin II in the early obstruction-induced activation of renal Ras. Furthermore, upstream inhibition of Ras signalling by blocking either angiotensin AT1 type receptor or by inhibiting Ras prenylation (atorvastatin, FTI o ChA) reduced the activation of the Ras/Erk/Akt signaling system and decreased the early fibrotic response in the obstructed kidney. This study points out that pharmacological inhibition of Ras activation may hold promise as a future strategy in the prevention of renal fibrosis. | - |
dc.description.sponsorship | This study was supported by grants from Ministerio de Economía y Competitividad (Grant SAF2010-15881 and Red de Investigacion Cooperativa en Enfermedades Renales REDINREN RD12/0021/0032), Junta de Castilla y León (Grant SA 001/C05 and Excellence Group GR100), and REDINREN which is an initiative of the Instituto de Salud Carlos III of Spain supported by FEDER funds. When performing the present study, Ana B. Rodríguez-Pena was a fellow of the Fundacion Renal “Iñigo Ávarez de Toledo” and Neil G. Docherty was a fellow ofThe Marie Curie Programme, EU. | - |
dc.publisher | Hindawi Publishing Corporation | - |
dc.relation.isversionof | Publisher's version | - |
dc.rights | openAccess | - |
dc.title | Effect of angiotensin II and small GTPase Ras signaling pathway inhibition on early renal changes in a murine model of obstructive nephropathy | - |
dc.type | artículo | - |
dc.identifier.doi | 10.1155/2014/124902 | - |
dc.relation.publisherversion | http://dx.doi.org/10.1155/2014/124902 | - |
dc.date.updated | 2016-03-18T12:18:27Z | - |
dc.description.version | Peer Reviewed | - |
dc.language.rfc3066 | eng | - |
dc.rights.license | http://creativecommons.org/licenses/by/3.0/ | - |
dc.contributor.funder | Junta de Castilla y León | - |
dc.contributor.funder | Fundación Renal Íñigo Álvarez de Toledo | - |
dc.contributor.funder | Federación Española de Enfermedades Raras | - |
dc.contributor.funder | European Commission | - |
dc.contributor.funder | Ministerio de Economía y Competitividad (España) | - |
dc.contributor.funder | Red Española de Investigación Renal | - |
dc.contributor.funder | Instituto de Salud Carlos III | - |
dc.relation.csic | Sí | - |
dc.identifier.funder | http://dx.doi.org/10.13039/501100002924 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100000780 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100003329 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100004587 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100014180 | es_ES |
dc.identifier.pmid | 25101263 | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | With Fulltext | - |
item.cerifentitytype | Publications | - |
item.openairetype | artículo | - |
item.grantfulltext | open | - |
Aparece en las colecciones: | (IBMCC) Artículos |
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Effect of Angiotensin II.pdf | 3,56 MB | Adobe PDF | Visualizar/Abrir |
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