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PLoS One. 2009;4(4):e5406. doi: 10.1371/journal.pone.0005406. Epub 2009 Apr 30.

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

Author information

1
Cellular Biology in Renal Diseases Laboratory, Fundación Jimenez Diaz, Universidad Autónoma Madrid, Madrid, Spain.

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-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.

PMID:
19404405
PMCID:
PMC2672164
DOI:
10.1371/journal.pone.0005406
[Indexed for MEDLINE]
Free PMC Article

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