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http://dx.doi.org/10.5483/BMBRep.2017.50.4.165

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))
Publication Information
BMB Reports / v.50, no.4, 2017 , pp. 208-213 More about this Journal
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
Cardiac hypertrophy; cGMP-dependent protein kinase-1; MicroRNA; Neonatal rat ventricular myocytes; Vascular endothelial growth factor signaling;
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