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miR-374 promotes myocardial hypertrophy by negatively regulating vascular endothelial growth factor receptor-1
Jong Sub Lee1, Dong Woo Song1, Jei Hyoung Park1
1School of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju 61005, Korea.
Insights
MicroRNA-374 promotes cardiac hypertrophy by inhibiting VEGFR1-mediated regression pathways. This study identifies miR-374 as a novel pro-hypertrophic factor in heart cells.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- MicroRNA Research
Background:
- Vascular Endothelial Growth Factor (VEGF) signaling influences blood vessel formation and cardiac hypertrophy.
- VEGF/VEGF-receptor-1 (VEGFR1) signaling promotes regression of cardiac hypertrophy.
- VEGF/VEGFR2 signaling is linked to cardiac hypertrophy.
Purpose of the Study:
- To investigate the role of microRNA-374 (miR-374) in cardiac hypertrophy.
- To elucidate the molecular mechanisms by which miR-374 affects cardiac hypertrophy pathways.
Main Methods:
- Neonatal rat ventricular myocytes (NRVMs) were used to study miR-374.
- Overexpression of miR-374 was performed.
- Luciferase assays were conducted to identify direct targets of miR-374.
Main Results:
- Overexpression of miR-374 activated G protein-coupled receptor-mediated prohypertrophic pathways.
- miR-374 inhibited VEGFR1-dependent regression pathways.
- miR-374 was found to directly target VEGFR1 and cGMP-dependent protein kinase-1.
Conclusions:
- miR-374 acts as a novel pro-hypertrophic microRNA.
- miR-374 suppresses the VEGFR1-mediated regression pathway in cardiac hypertrophy.
- These findings provide insights into microRNA regulation of cardiac remodeling.
Abstract:
Vascular endothelial growth factor (VEGF) is an essential cytokine that has functions in the formation of new blood vessels and regression of cardiac hypertrophy. VEGF/VEGF-receptor-1 (VEGFR1) signaling plays a key role in the regression of cardiac hypertrophy, whereas VEGF/VEGFR2 signaling leads to cardiac hypertrophy. In this study, we identified the prohypertrophic role of miR-374 using neonatal rat ventricular myocytes (NRVMs). Our results showed that overexpression of miR-374 activated G protein-coupled receptor-mediated prohypertrophic pathways by the inhibition of VEGFR1-dependent regression pathways. Luciferase assays revealed that miR-374 could directly target the 3'-untranslated regions of VEGFR1 and cGMP-dependent protein kinase-1. Collectively, these findings demonstrated that miR-374 was a novel pro-hypertrophic microRNA functioning to suppress the VEGFR1-mediated regression pathway. [BMB Reports 2017; 50(4): 208-213].
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