Sphingosine-1-phosphate (S1P), a bioactive sphingolipid, is recognized as a critical regulator\nin physiological and pathophysiological processes of atherosclerosis (AS). However, the underlying\nmechanism remains unclear. As the precursor cells of endothelial cells (ECs), endothelial progenitor\ncells (EPCs) can prevent AS development through repairing endothelial monolayer impaired by\nproatherogenic factors. The present study investigated the effects of S1P on the biological features of\nmouse bone marrow-derived EPCs and the underlying mechanism. The results showed that S1P\nimproved cell viability, adhesion, and nitric oxide (NO) release of EPCs in a bell-shaped manner,\nand migration and tube formation dose-dependently. The aforementioned beneficial eects of S1P\non EPCs could be inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitor of LY294002 and\nnitric oxide synthase (NOS) inhibitor of Nâ??-nitro-L-arginine-methyl ester hydrochloride (L-NAME).\nThe inhibitor of LY294002 inhibited S1P-stimulated activation of phosphorylated protein kinase B\n(AKT) (p-AKT) and endothelial nitric oxide synthase (eNOS) (p-eNOS), and down-regulated the level\nof eNOS significantly. The results suggest that S1P improves the biological features of EPCs partially\nthrough PI3K/AKT/eNOS/NO signaling pathway.
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