Abstract
Our group previously demonstrated the suppressive effect of glucagon-like peptide-1(GLP-1)on macrophage-driven atherosclerosis in apolipoprotein E-de�- cient (apoE / )mice. In the present study we investigated the suppressive effect of GLP-1 on the atherogenic phenotype of vascular smooth muscle cells(VSMCs) in vivo using apoE / mice, and the proliferation and migration of human VSMCs in vitro. A 4-week infusion of GLP-1 in 17-week-old apoE / mice significantly reduced the proliferative VSMC phenotype stained with SMemb. Platelet-derived growth factor(PDGF) -BB signicantly stimulated the proliferation of human aortic VSMCs by three fold. Both 0.1 and 1 nmol / l GLP-1 signicantly suppressed the PDGF-induced VSMC proliferation, and this suppressive effect was significantly abolished by the GLP-1 receptor antagonist exendin(9−39)(50 nmol / l) . The GLP-1 receptor agonists liraglutide(100 nmol / l)and exendin-4(100 nmol / l)mim- icked GLP-1, signicantly suppressing PDGF-induced VSMC proliferation. PDGF- BB signicantly stimulated the migration of human aortic VSMCs by 1.7 -fold, and this effect was signicantly suppressed by 1 nmol / l GLP-1. Thesendings suggest that GLP-1-related treatments may prevent the progression of atherosclerotic lesions by suppressing the proliferation and migration of VSMCs, which are characteristic features of atherosclerosis.
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