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

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RGS1 regulates myeloid cell accumulation in atherosclerosis and aortic aneurysm rupture through altered chemokine signalling. / Patel, Jyoti; McNeill, Eileen; Douglas, Gillian; Hale, Ashley B; de Bono, Joseph; Lee, Regent; Iqbal, Asif Jilani; Regan-Komito, Daniel; Stylianou, Elena; Greaves, David R; Channon, Keith M.

In: Nature Communications, Vol. 6, 18.03.2015, p. 6614.

Research output: Contribution to journalArticlepeer-review

Harvard

Patel, J, McNeill, E, Douglas, G, Hale, AB, de Bono, J, Lee, R, Iqbal, AJ, Regan-Komito, D, Stylianou, E, Greaves, DR & Channon, KM 2015, 'RGS1 regulates myeloid cell accumulation in atherosclerosis and aortic aneurysm rupture through altered chemokine signalling', Nature Communications, vol. 6, pp. 6614. https://doi.org/10.1038/ncomms7614

APA

Patel, J., McNeill, E., Douglas, G., Hale, A. B., de Bono, J., Lee, R., Iqbal, A. J., Regan-Komito, D., Stylianou, E., Greaves, D. R., & Channon, K. M. (2015). RGS1 regulates myeloid cell accumulation in atherosclerosis and aortic aneurysm rupture through altered chemokine signalling. Nature Communications, 6, 6614. https://doi.org/10.1038/ncomms7614

Vancouver

Author

Patel, Jyoti ; McNeill, Eileen ; Douglas, Gillian ; Hale, Ashley B ; de Bono, Joseph ; Lee, Regent ; Iqbal, Asif Jilani ; Regan-Komito, Daniel ; Stylianou, Elena ; Greaves, David R ; Channon, Keith M. / RGS1 regulates myeloid cell accumulation in atherosclerosis and aortic aneurysm rupture through altered chemokine signalling. In: Nature Communications. 2015 ; Vol. 6. pp. 6614.

Bibtex

@article{8dd524f84b7e45469469620897fbe061,
title = "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.",
keywords = "Animals, Aorta, Aortic Aneurysm, Atherosclerosis, Blood Pressure, Bone Marrow Transplantation, Chemokines, Chemotaxis, Flow Cytometry, Humans, Inflammation, Leukocytes, Macrophages, Male, Mice, Mice, Knockout, Monocytes, RGS Proteins, Receptors, Chemokine, Signal Transduction, Vascular Diseases, Journal Article, Research Support, Non-U.S. Gov't",
author = "Jyoti Patel and Eileen McNeill and Gillian Douglas and Hale, {Ashley B} and {de Bono}, Joseph and Regent Lee and Iqbal, {Asif Jilani} and Daniel Regan-Komito and Elena Stylianou and Greaves, {David R} and Channon, {Keith M}",
year = "2015",
month = mar,
day = "18",
doi = "10.1038/ncomms7614",
language = "English",
volume = "6",
pages = "6614",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Springer",

}

RIS

TY - JOUR

T1 - RGS1 regulates myeloid cell accumulation in atherosclerosis and aortic aneurysm rupture through altered chemokine signalling

AU - Patel, Jyoti

AU - McNeill, Eileen

AU - Douglas, Gillian

AU - Hale, Ashley B

AU - de Bono, Joseph

AU - Lee, Regent

AU - Iqbal, Asif Jilani

AU - Regan-Komito, Daniel

AU - Stylianou, Elena

AU - Greaves, David R

AU - Channon, Keith M

PY - 2015/3/18

Y1 - 2015/3/18

N2 - 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.

AB - 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.

KW - Animals

KW - Aorta

KW - Aortic Aneurysm

KW - Atherosclerosis

KW - Blood Pressure

KW - Bone Marrow Transplantation

KW - Chemokines

KW - Chemotaxis

KW - Flow Cytometry

KW - Humans

KW - Inflammation

KW - Leukocytes

KW - Macrophages

KW - Male

KW - Mice

KW - Mice, Knockout

KW - Monocytes

KW - RGS Proteins

KW - Receptors, Chemokine

KW - Signal Transduction

KW - Vascular Diseases

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1038/ncomms7614

DO - 10.1038/ncomms7614

M3 - Article

C2 - 25782711

VL - 6

SP - 6614

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

ER -