Sphingosine-1-phosphate-induced smooth muscle cell migration involves the mammalian target of rapamycin

S-1-P is released from activated platelets at sites of vessel injury and contributes to the development of intimal hyperplasia after bypass grafting, angioplasty, and stenting. S-1-P is a potent pro-migratory molecule for SMCs. Rapamycin is a commonly used immunosuppressive agent that has most recently been incorporated as the biologic agent in drug eluting stents with good success in the coronary circulation. Rapamycin inhibits the mammalian target of rapamycin, which, in turn, controls the translational mechanisms of the cell. The role of translational control during S-1-P-induced SMC migration is poorly understood. This study identifies a link between the mammalian target of rapamycin translational pathway and S-1-P and demonstrates how rapamycin might interfere with another facet of a vessel's response to injury after a vascular intervention, namely by interfering with the cell signaling of factors released from platelets deposited at the injury site.