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Role of the receptor Mas in macrophage-mediated inflammation in vivo

Item Type:Article
Title:Role of the receptor Mas in macrophage-mediated inflammation in vivo
Creators Name:Hammer, A. and Yang, G. and Friedrich, J. and Kovacs, A. and Lee, D.H. and Grave, K. and Jörg, S. and Alenina, N. and Grosch, J. and Winkler, J. and Gold, R. and Bader, M. and Manzel, A. and Rump, L.C. and Müller, D.N. and Linker, R.A. and Stegbauer, J.
Abstract:Recently, an alternative renin-angiotensin system pathway has been described, which involves binding of angiotensin-(1-7) to its receptor Mas. The Mas axis may counterbalance angiotensin-II-mediated proinflammatory effects, likely by affecting macrophage function. Here we investigate the role of Mas in murine models of autoimmune neuroinflammation and atherosclerosis, which both involve macrophage-driven pathomechanisms. Mas signaling affected macrophage polarization, migration, and macrophage-mediated T-cell activation. Mas deficiency exacerbated the course of experimental autoimmune encephalomyelitis and increased macrophage infiltration as well as proinflammatory gene expression in the spleen and spinal cord. Furthermore, Mas deficiency promoted atherosclerosis by affecting macrophage infiltration and migration and led to increased oxidative stress as well as impaired endothelial function in ApoE-deficient mice. In summary, we identified the Mas axis as an important factor in macrophage function during inflammation of the central nervous and vascular system in vivo. Modulating the Mas axis may constitute an interesting therapeutic target in multiple sclerosis and/or atherosclerosis.
Keywords:Atherosclerosis, EAE, Inflammation, Macrophages, Renin-Angiotensin System, Animals, Mice
Source:Proceedings of the National Academy of Sciences of the United States of America
Publisher:National Academy of Sciences
Page Range:14109-14114
Date:6 December 2016
Official Publication:https://doi.org/10.1073/pnas.1612668113
PubMed:View item in PubMed

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