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http://hdl.handle.net/10261/135675
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dc.contributor.author | Fabbiano, Salvatore | - |
dc.contributor.author | Menacho-Márquez, Mauricio | - |
dc.contributor.author | Robles-Valero, Javier | - |
dc.contributor.author | Pericacho, Miguel | - |
dc.contributor.author | Matesanz-Marín, Adela | - |
dc.contributor.author | García-Macías, Carmen | - |
dc.contributor.author | Sevilla, Mª Ángeles | - |
dc.contributor.author | Montero, María J. | - |
dc.contributor.author | Alarcón, Balbino | - |
dc.contributor.author | López-Novoa, José M. | - |
dc.contributor.author | Martín, Pilar | - |
dc.contributor.author | Bustelo, Xosé R. | - |
dc.date.accessioned | 2016-08-19T10:31:28Z | - |
dc.date.available | 2016-08-19T10:31:28Z | - |
dc.date.issued | 2015 | - |
dc.identifier | doi: 10.1128/MCB.00518-15 | - |
dc.identifier | e-issn: 1098-5549 | - |
dc.identifier | issn: 0270-7306 | - |
dc.identifier.citation | Molecular and Cellular Biology 35(20): 3528-3546 (2015) | - |
dc.identifier.uri | http://hdl.handle.net/10261/135675 | - |
dc.description.abstract | Hypertension-associated cardiorenal diseases represent one of the heaviest burdens for current health systems. In addition to hemodynamic damage, recent results have revealed that hematopoietic cells contribute to the development of these diseases by generating proinflammatory and profibrotic environments in the heart and kidney. However, the cell subtypes involved remain poorly characterized. Here we report that CD39+ regulatory T (TREG) cells utilize an immunosuppression-independent mechanism to counteract renal and possibly cardiac damage during angiotensin II (AngII)-dependent hypertension. This mechanism relies on the direct apoptosis of tissue-resident neutrophils by the ecto-ATP diphosphohydrolase activity of CD39. In agreement with this, experimental and genetic alterations in TREG/TH cell ratios have a direct impact on tissue-resident neutrophil numbers, cardiomyocyte hypertrophy, cardiorenal fibrosis, and, to a lesser extent, arterial pressure elevation during AngII-driven hypertension. These results indicate that TREG cells constitute a first protective barrier against hypertension-driven tissue fibrosis and, in addition, suggest new therapeutic avenues to prevent hypertension-linked cardiorenal diseases. | - |
dc.description.sponsorship | This work has been supported by grants from the Castilla-León Autonomous Government (CSI101U13), the Spanish Ministry of Economy and Competitiveness (SAF2012-31371, RD12/0036/0002), Worldwide Cancer Research, the Solórzano Foundation, and the Ramón Areces Foundation to X.R.B. P.M. is funded by the Spanish Ministry of Economy and Competitiveness (SAF2011-27330). S.F., M.M.-M., J.R.-V., and A.M.-M. were supported by the Spanish Ministry of Economy and Competitiveness through BES-2010-031386, CSIC JAE-Doc, Juan de la Cierva, and BES-2009-016103 contracts, respectively. Spanish government-sponsored funding to X.R.B. is partially supported by the European Regional Development Fund. | - |
dc.publisher | American Society for Microbiology | - |
dc.relation.isversionof | Postprint | - |
dc.rights | openAccess | - |
dc.title | Immunosuppression-independent role of regulatory T cells against hypertension-driven renal dysfunctions | - |
dc.type | artículo | - |
dc.identifier.doi | 10.1128/MCB.00518-15 | - |
dc.relation.publisherversion | http://dx.doi.org/10.1128/MCB.00518-15 | - |
dc.date.updated | 2016-08-19T10:31:28Z | - |
dc.description.version | Peer Reviewed | - |
dc.language.rfc3066 | eng | - |
dc.contributor.funder | Junta de Castilla y León | - |
dc.contributor.funder | Worldwide Cancer Research | - |
dc.contributor.funder | Fundación Memoria de D. Samuel Solorzano Barruso | - |
dc.contributor.funder | Fundación Ramón Areces | - |
dc.contributor.funder | Consejo Superior de Investigaciones Científicas (España) | - |
dc.contributor.funder | European Commission | - |
dc.contributor.funder | Ministerio de Economía y Competitividad (España) | - |
dc.relation.csic | Sí | - |
dc.identifier.funder | http://dx.doi.org/10.13039/501100007287 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/100008054 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100003339 | 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/10.13039/501100014180 | es_ES |
dc.identifier.pmid | 26240279 | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.fulltext | With Fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.openairetype | artículo | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | open | - |
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