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Abstract
The effects of serotonin on migration of cultured rat aortic smooth muscle cells (SMC)
were studied to clarify the role of this substance in the pathogenesis of atherosclerosis.
Serotonin alone did not stimulate SMC migration but stimulated it at physiological
concentrations in the presence of other migration factors such as SMC-derived migration
factor, platelet-derived migration factor and fibronectin. Checker-board analysis
revealed that the serotonin effect was chemotactic. Moreover, serotonin effects were
completely abolished by a selective inhibitor of the 5-HT2 receptor (MCI-9042), indicating
that serotonin effects were mediated through the 5-HT2 receptor pathway. Finally,
serotonin effects were also abolished by a phospholipase C inhibitor, U73122, suggesting
that the 5-HT2 receptor mediated signal of serotonin was transduced by PLC. The results
suggest that platelet-derived serotonin plays some role in the SMC dominant neointima
formation.