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miR-374 promotes myocardial hypertrophy by negatively regulating vascular endothelial growth factor receptor-1 signaling

  • Lee, Jong Sub (School of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST)) ;
  • Song, Dong Woo (School of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST)) ;
  • Park, Jei Hyoung (School of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST)) ;
  • Kim, Jin Ock (School of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST)) ;
  • Cho, Chunghee (School of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST)) ;
  • Kim, Do Han (School of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST))
  • Received : 2016.09.27
  • Accepted : 2016.10.28
  • Published : 2017.04.30

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.

Keywords

References

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