School of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju 61005, Korea.
BMB Rep. 2017 Apr;50(4):208-213. doi: 10.5483/bmbrep.2017.50.4.165.
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].
血管内皮生长因子 (VEGF) 是一种重要的细胞因子，具有形成新血管和心脏肥大退化的功能。VEGF/VEGF 受体-1 (VEGFR1) 信号转导在心脏肥大的退化中起着关键作用，而 VEGF/VEGFR2 信号转导则导致心脏肥大。在这项研究中，我们使用新生大鼠心室肌细胞 (NRVM) 鉴定了 miR-374 的促肥大作用。结果表明，miR-374 的过表达通过抑制 VEGFR1 依赖性退化途径激活了 G 蛋白偶联受体介导的促肥大途径。荧光素酶检测表明，miR-374 可以直接靶向 VEGFR1 和 cGMP 依赖性蛋白激酶-1 的 3'非翻译区。总之，这些发现表明 miR-374 是一种新型的促肥大 microRNA，可抑制 VEGFR1 介导的退化途径。[BMB 报告 2017;50(4):208-213]。
