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

Jyoti Patel (), Eileen McNeill, Gillian Douglas, Ashley B. Hale, Joseph de Bono, Regent Lee, Asif J. Iqbal, Daniel Regan-Komito, Elena Stylianou, David R. Greaves and Keith M. Channon ()
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Jyoti Patel: British Heart Foundation Centre of Research Excellence, University of Oxford, John Radcliffe Hospital
Eileen McNeill: British Heart Foundation Centre of Research Excellence, University of Oxford, John Radcliffe Hospital
Gillian Douglas: British Heart Foundation Centre of Research Excellence, University of Oxford, John Radcliffe Hospital
Ashley B. Hale: British Heart Foundation Centre of Research Excellence, University of Oxford, John Radcliffe Hospital
Joseph de Bono: British Heart Foundation Centre of Research Excellence, University of Oxford, John Radcliffe Hospital
Regent Lee: British Heart Foundation Centre of Research Excellence, University of Oxford, John Radcliffe Hospital
Asif J. Iqbal: Sir William Dunn School of Pathology, University of Oxford
Daniel Regan-Komito: Sir William Dunn School of Pathology, University of Oxford
Elena Stylianou: Jenner Institute, University of Oxford
David R. Greaves: Sir William Dunn School of Pathology, University of Oxford
Keith M. Channon: British Heart Foundation Centre of Research Excellence, University of Oxford, John Radcliffe Hospital

Nature Communications, 2015, vol. 6, issue 1, 1-11

Abstract: Abstract 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.

Date: 2015
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DOI: 10.1038/ncomms7614

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