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FGFR1 forms an FRS2-dependent complex with mTOR to regulate smooth muscle marker gene expression
1Center for Molecular Medicine, Maine Medical Center Research Institute, Scarborough, ME 04074-7205, USA. chenp@mmc.org
Biochemical and Biophysical Research Communications
|March 17, 2009
Summary
Fibroblast growth factor receptor-1 (FGFR1) activates the Akt/mTOR pathway, influencing vascular smooth muscle cell (VSMC) phenotype. Inhibiting mTOR partially reversed FGFR1-induced changes, suggesting a therapeutic target for cardiovascular diseases.
Area of Science:
- Cardiovascular Biology
- Cell Signaling
- Molecular Medicine
Background:
- Vascular smooth muscle cells (VSMCs) undergo phenotypic switching in cardiovascular diseases like atherosclerosis.
- This switch involves reduced contractile proteins and increased growth factor receptor expression.
- Fibroblast growth factor receptor-1 (FGFR1) signaling is implicated in VSMC phenotypic modulation.
Purpose of the Study:
- To investigate the downstream signaling pathway of FGFR1 in regulating smooth muscle (SM) marker gene expression.
- To elucidate the role of the Akt/mTOR pathway in FGFR1-mediated VSMC phenotypic changes.
Main Methods:
- Examined FGFR1 signaling in VSMCs.
- Utilized the mTOR inhibitor rapamycin.
- Investigated the interaction between mTOR and FGFR1 using co-immunoprecipitation.
Main Results:
- FGFR1 activation led to the activation of the Akt/mTOR pathway.
- Rapamycin partially reversed the downregulation of SM marker genes induced by FGFR1.
- mTOR was found to form a multi-protein complex with FGFR1 in VSMCs.
Conclusions:
- FGFR1 signaling regulates VSMC phenotype through the Akt/mTOR pathway.
- Targeting the mTOR pathway may offer therapeutic potential for cardiovascular diseases.
- The interaction between mTOR and FGFR1 is a key component of this signaling axis.
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