Angiotensin-(1-7) and the G protein-coupled receptor Mas are key players in renal inflammation

Vanesa Esteban*, Silvia Heringer-Walther, Anja Sterner-Kock, Ron de Bruin, Sandra van den Engel, Yong Wang, Sergio Mezzano, Jesus Egido, Heinz Peter Schultheiss, Marta Ruiz-Ortega, Thomas Walther*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

113 Citations (Scopus)
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Abstract

Angiotensin (Ang) II mediates pathophysiologial changes in the kidney. Ang-(1-7) by interacting with the G protein-coupled receptor Mas may also have important biological activities. In this study, renal deficiency for Mas diminished renal damage in models of renal insufficiency as unilateral ureteral obstruction and ischemia/reperfusion injury while the infusion of Ang-(1-7) to wild-type mice pronounced the pathological outcome by aggravating the inflammatory response. Mas deficiency inhibited NF-κB activation and thus the elevation of inflammation-stimulating cytokines, while Ang-(1-7) infusion had proinflammatory properties in experimental models of renal failure as well as under basal conditions. The Ang-(1-7)-mediated NF-κB activation was Mas dependent but did not involve Ang II receptors. Therefore, the blockade of the NF-κB-activating properties of the receptor Mas could be a new strategy in the therapy of failing kidney.

Original languageEnglish
Article numbere5406
JournalPLoS ONE
Volume4
Issue number4
DOIs
Publication statusPublished - 30 Apr 2009

Bibliographical note

Funding:
This work has been supported by grants from the Nierstichting Nederland (C04.2103), Ministerio de Educacion y Ciencia (SAF 2005-03378), Comunidad
de Madrid (11/BCB/016), Ministerio de Ciencia y Tecnologı´a (HA2004-0006), Ministerio de Sanidad (ISCIII-RETIC RD06/0016/0004). The funders had no role in study
design, data collection and analysis, decision to publish, or preparation of the manuscript

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