| Summary: | 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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