Novel aspects of chemokine receptor signalling in cardiovascular inflammation

The regulation of monocyte recruitment and macrophage retention into the vascular wall and heart are critical in the progression of cardiovascular disease but also to repair and remodelling after myocardial infarction (MI). Chemokines regulate leukocyte recruitment through G-protein coupled receptor...

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Главные авторы: Patel, J, Rohling, M, Smart, N, Choudhury, R, Greaves, D, Riley, P, Channon, K
Формат: Conference item
Опубликовано: Oxford University Press 2018
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author Patel, J
Rohling, M
Smart, N
Choudhury, R
Greaves, D
Riley, P
Channon, K
author_facet Patel, J
Rohling, M
Smart, N
Choudhury, R
Greaves, D
Riley, P
Channon, K
author_sort Patel, J
collection OXFORD
description The regulation of monocyte recruitment and macrophage retention into the vascular wall and heart are critical in the progression of cardiovascular disease but also to repair and remodelling after myocardial infarction (MI). Chemokines regulate leukocyte recruitment through G-protein coupled receptor (GPCR) signalling. Although chemokine signalling is a rational therapeutic target in MI, redundancy within the system limits the potential utility of targeting individual chemokines. Downstream modulators such as Regulator of G-Protein Signalling (RGS) proteins, deactivate GPCR signalling by stimulating GTPase activity of the α-subunit. We have found that RGS1 modulates leukocyte chemotactic signalling and regulates leukocyte accumulation in atherosclerosis and aortic aneurysm formation. Rgs1 expression is upregulated in activated inflammatory cells where it functions to inhibit migration, thus promoting inflammation by retention and accumulation of leukocytes, whereas Rgs1-deficiency confers protection.
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spelling oxford-uuid:9fe28796-e4b4-47f0-b5d2-fc63d2c3a4082022-03-27T02:01:30ZNovel aspects of chemokine receptor signalling in cardiovascular inflammationConference itemhttp://purl.org/coar/resource_type/c_5794uuid:9fe28796-e4b4-47f0-b5d2-fc63d2c3a408Symplectic Elements at OxfordOxford University Press2018Patel, JRohling, MSmart, NChoudhury, RGreaves, DRiley, PChannon, KThe regulation of monocyte recruitment and macrophage retention into the vascular wall and heart are critical in the progression of cardiovascular disease but also to repair and remodelling after myocardial infarction (MI). Chemokines regulate leukocyte recruitment through G-protein coupled receptor (GPCR) signalling. Although chemokine signalling is a rational therapeutic target in MI, redundancy within the system limits the potential utility of targeting individual chemokines. Downstream modulators such as Regulator of G-Protein Signalling (RGS) proteins, deactivate GPCR signalling by stimulating GTPase activity of the α-subunit. We have found that RGS1 modulates leukocyte chemotactic signalling and regulates leukocyte accumulation in atherosclerosis and aortic aneurysm formation. Rgs1 expression is upregulated in activated inflammatory cells where it functions to inhibit migration, thus promoting inflammation by retention and accumulation of leukocytes, whereas Rgs1-deficiency confers protection.
spellingShingle Patel, J
Rohling, M
Smart, N
Choudhury, R
Greaves, D
Riley, P
Channon, K
Novel aspects of chemokine receptor signalling in cardiovascular inflammation
title Novel aspects of chemokine receptor signalling in cardiovascular inflammation
title_full Novel aspects of chemokine receptor signalling in cardiovascular inflammation
title_fullStr Novel aspects of chemokine receptor signalling in cardiovascular inflammation
title_full_unstemmed Novel aspects of chemokine receptor signalling in cardiovascular inflammation
title_short Novel aspects of chemokine receptor signalling in cardiovascular inflammation
title_sort novel aspects of chemokine receptor signalling in cardiovascular inflammation
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AT rohlingm novelaspectsofchemokinereceptorsignallingincardiovascularinflammation
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AT choudhuryr novelaspectsofchemokinereceptorsignallingincardiovascularinflammation
AT greavesd novelaspectsofchemokinereceptorsignallingincardiovascularinflammation
AT rileyp novelaspectsofchemokinereceptorsignallingincardiovascularinflammation
AT channonk novelaspectsofchemokinereceptorsignallingincardiovascularinflammation