Arterioscler Thromb Vasc Biol 2013 Oct 15;33(10):2415-24. Epub 2013 Aug 15.
From the Department of Medicine and Surgery, University of Salerno, Salerno, Italy (M.C., E.C., G.l.); Department of Pharmacology, Center for Translational Medicine, Temple University, Philadelphia, PA (M.C.); Department of Biomedical Sciences, University of Naples Federico II, Naples, Italy (D.S., A.F., C.D.G., R.A., M.G.M., B.T.); Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO (G.W.D.); and IRCCS Multimedica, Milan, Italy (G.I.).
Objective: The role of endothelial G protein-coupled receptor kinase 2 (GRK2) was investigated in mice with selective deletion of the kinase in the endothelium (Tie2-CRE/GRK2(fl/fl)).
Approach And Results: Aortas from Tie2-CRE/GRK2(fl/fl) presented functional and structural alterations as compared with control GRK2(fl/fl) mice. In particular, vasoconstriction was blunted to different agonists, and collagen and elastic rearrangement and macrophage infiltration were observed. In primary cultured endothelial cells deficient for GRK2, mitochondrial reactive oxygen species was increased, leading to expression of cytokines. Chronic treatment with a reactive oxygen species scavenger in mice corrected the vascular phenotype by recovering vasoconstriction, structural abnormalities, and reducing macrophage infiltration.
Conclusions: These results demonstrate that GRK2 removal compromises vascular phenotype and integrity by increasing endothelial reactive oxygen species production.
A mutation of the beta 2-adrenergic receptor impairs agonist activation of adenylyl cyclase without affecting high affinity agonist binding. Distinct molecular determinants of the receptor are involved in physical coupling to and functional activation of Gs. Hausdorff WP et al. J Biol Chem 1990
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