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S1P2/G12/13 Signaling Negatively Regulates Macrophage Activation and Indirectly Shapes the Atheroprotective B1-Cell Population. | LitMetric

S1P2/G12/13 Signaling Negatively Regulates Macrophage Activation and Indirectly Shapes the Atheroprotective B1-Cell Population.

Arterioscler Thromb Vasc Biol

From the Department of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany (M.G., D.T., K.T., J.A.J., K.K.S., N.W.); Pharmazentrum Frankfurt/ZAFES, Clinical Pharmacology (N.F.B., G.G.) and Centre for Molecular Medicine, Medical Faculty (N.W.), J.W. Goethe University Frankfurt, Frankfurt, Germany; and Department of Laboratory Medicine, Medical University of Vienna and Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria (C.J.B.).

Published: January 2016

AI Article Synopsis

Article Abstract

Objectives: Monocyte/macrophage recruitment and activation at vascular predilection sites plays a central role in the pathogenesis of atherosclerosis. Heterotrimeric G proteins of the G12/13 family have been implicated in the control of migration and inflammatory gene expression, but their function in myeloid cells, especially during atherogenesis, is unknown.

Approach And Results: Mice with myeloid-specific deficiency for G12/13 show reduced atherosclerosis with a clear shift to anti-inflammatory gene expression in aortal macrophages. These changes are because of neither altered monocyte/macrophage migration nor reduced activation of inflammatory gene expression; on the contrary, G12/13-deficient macrophages show an increased nuclear factor-κB-dependent gene expression in the resting state. Chronically increased inflammatory gene expression in resident peritoneal macrophages results in myeloid-specific G12/13-deficient mice in an altered peritoneal micromilieu with secondary expansion of peritoneal B1 cells. Titers of B1-derived atheroprotective antibodies are increased, and adoptive transfer of peritoneal cells from mutant mice conveys atheroprotection to wild-type mice. With respect to the mechanism of G12/13-mediated transcriptional control, we identify an autocrine feedback loop that suppresses nuclear factor-κB-dependent gene expression through a signaling cascade involving sphingosine 1-phosphate receptor subtype 2, G12/13, and RhoA.

Conclusions: Together, these data show that selective inhibition of G12/13 signaling in macrophages can augment atheroprotective B-cell populations and ameliorate atherosclerosis.

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Source
http://dx.doi.org/10.1161/ATVBAHA.115.306066DOI Listing

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