Angiotensin-(1-7) and the g protein-coupled receptor MAS are key players in renal inflammation.

• Main Authors: 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
• Format: Article
• Language: English
• Published: Public Library of Science (PLoS) 2009-01-01
• Series: PLoS ONE
• Online Access: http://europepmc.org/articles/PMC2672164?pdf=render

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-kappaB 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-kappaB activation was Mas dependent but did not involve Ang II receptors. Therefore, the blockade of the NF-kappaB-activating properties of the receptor Mas could be a new strategy in the therapy of failing kidney.