Journal
NATURE COMMUNICATIONS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms7614
Keywords
-
Categories
Funding
- British Heart Foundation [RG/10/15/28578, RG/12/5/29576]
- Wellcome Trust [091504/Z/10/Z, 090532/Z/09/Z]
- National Institute for Health Research (NIHR) Oxford Biomedical Research Centre
- Wellcome Trust [091504/Z/10/Z] Funding Source: Wellcome Trust
- British Heart Foundation [RG/10/15/28578, RG/12/5/29576, PG/15/35/31403] Funding Source: researchfish
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available