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Angiotensin-(1-7) and the G protein-coupled receptor Mas are key players in renal inflammation
Keywords: model, disorder, proteins, mouse, animals, cytokines, cytokine, binding, kidney, inflammation, protein, injury, cell, disease, pathogenesis, mutant, peptide, mice, ischemia, experiment, diseases, receptor, agents, fragments, failure, oncogene, angiotensin, interaction, agent, tissue, reperfusion, drug, pathology, antagonism, obstruction, article, enhancer, fragment, oncoprotein, nephritis, function, immunoglobulin, nf-kappa, ureter, mas, type, controlled, animal, knockout, c, wild, study, 1, induced, nonhuman, Receptors,, (1, chemically, Proto-Oncogene, I, G, antihypertensive, Mice,, unclassified, b, G-Protein-Coupled, Mus, coupled, proto, angiotensin[1-7], 7), (1-7), c-mas-1
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-?B 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-?B activation was Mas dependent but did not involve Ang II receptors. Therefore, the blockade of the NF-?B-activating properties of the receptor Mas could be a new strategy in the therapy of failing kidney. © 2009 Esteban et al.
Más información
| Título según SCOPUS: | Angiotensin-(1-7) and the G protein-coupled receptor Mas are key players in renal inflammation |
| Título de la Revista: | PLOS ONE |
| Volumen: | 4 |
| Número: | 4 |
| Editorial: | PUBLIC LIBRARY SCIENCE |
| Fecha de publicación: | 2009 |
| URL: | http://www.scopus.com/inward/record.url?eid=2-s2.0-65549108738&partnerID=q2rCbXpz |
| DOI: |
10.1371/journal.pone.0005406 |
| Notas: | SCOPUS |