Journal article
RGS1 regulates myeloid cell accumulation in atherosclerosis and aortic aneurysm rupture through altered chemokine signalling
- 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.
- Publication status:
- Published
- Peer review status:
- Peer reviewed
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(Preview, Version of record, pdf, 1.7MB, Terms of use)
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- Publisher copy:
- 10.1038/ncomms7614
Authors
- Publisher:
- Nature Publishing Group
- Journal:
- Nature Communications More from this journal
- Volume:
- 6
- Issue:
- 1
- Article number:
- 6614
- Publication date:
- 2015-03-18
- Acceptance date:
- 2015-02-12
- DOI:
- EISSN:
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2041-1723
- ISSN:
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2041-1723
- Language:
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English
- Pubs id:
-
pubs:512811
- UUID:
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uuid:976c8bfe-97d8-45e8-b024-b659a28b4b02
- Local pid:
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pubs:512811
- Source identifiers:
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512811
- Deposit date:
-
2015-10-13
Terms of use
- Copyright holder:
- Macmillan Publishers Limited
- Copyright date:
- 2015
- Rights statement:
- © 2015 Macmillan Publishers Limited. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
- Licence:
- CC Attribution (CC BY)
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