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Chemokine signalling drives monocyte recruitment in atherosclerosis and aortic aneurysms. The mechanisms that lead to retention and accumulation of macrophages in the vascular wall remain unclear. Regulator of G-Protein Signalling-1 (RGS1) deactivates G-protein signalling, reducing the response to sustained chemokine stimulation. Here we show that  Rgs1  is upregulated in atherosclerotic plaque and aortic aneurysms.  Rgs1  reduces macrophage chemotaxis and desensitizes chemokine receptor signalling. In early atherosclerotic lesions,  Rgs1  regulates macrophage accumulation and is required for the formation and rupture of Angiotensin II-induced aortic aneurysms, through effects on leukocyte retention. Collectively, these data reveal a role for  Rgs1  in leukocyte trafficking and vascular inflammation and identify  Rgs1 , and inhibition of chemokine receptor signalling as potential therapeutic targets in vascular disease.

RGS1 regulates myeloid cell accumulation in atherosclerosis and aortic aneurysm rupture through altered chemokine signalling