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Abstract
Vascular smooth muscle cells (VSMCs) switch from a contractile to a synthetic phenotype
in human cardiovascular disease such as atherosclerosis and restenosis after angioplasty.
VSMCs show reduced expression of contractile proteins and are capable of responding
to mitogens by increasing expression of growth factor receptors. Fibroblast growth
factor receptor-1 (FGFR1) signaling is one of several signaling pathways involved
in this VSMC phenotypic switching. The aim of this study was to examine the signaling
pathway downstream of FGFR1 in the regulation of SM marker gene expression. We found
that FGFR1 activated Akt/mTOR pathway and that the mTOR inhibitor rapamycin partially
reversed FGFR1-mediated downregulation of SM marker gene expression. Furthermore,
we showed that mTOR forms a multi-protein complex with FGFR1 in VSMCs. These findings
provide novel information for future development of therapeutic strategies for the
treatment of human cardiovascular disease.