Glucagon-like peptide-1 receptor agonist reduces di(2-ethylhexyl) phthalate-induced atherosclerotic processes in vascular smooth muscle cells.

Glucagon-like peptide-1 receptor (GLP1R) agonist is an incretin hormone and regulates glucose metabolism. However, phthalates, known as endocrine disruptors, can interfere with hormone homeostasis. In the present study, we aimed to estimate the impact of GLP1R agonist on di(2 ethylhexyl) phthalate (DEHP)-induced atherosclerosis. For this purpose, the effects of GLP1R agonist on various atherogenesis-related cellular processes and pathways were assessed in vascular smooth muscle cells (VSMCs). DEHP-induced cell proliferation and migration were significantly decreased by GLP1R agonist in VSMCs. Protein levels of matrix metalloproteinase (MMP)-2 and MMP-9 were significantly decreased in cells exposed to GLP1R agonist, compared with DEHP-treated cells. Expression levels of intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 were also reduced in GLP1R agonist-treated cells. Similarly, DEHP-associated phosphorylation of protein kinase B and extracellular signal-regulated kinase 1/2 was decreased in GLP1R agonist-treated cells, compared with DEHP-treated cells. Our findings suggest that treatment with GLP1R agonist counteracts the activation of pathways related to atherosclerosis.