摘要
Background Cardiac hypertrophy is an adaptive enlargement of the myocardium in response to stress or inju- ry. Many studies have revealed that microRNAs participate in cardiac hypertrophy, but the role of microRNA-214 -3p （miR-214-3p） in cardiac hypertrophy has not been illustrated. The present study aimed to investigate the ex- pression and potential role of miR-214-3p in a mouse model of angiotensin-II （Ang-II） infusion-induced myocar- dium hypertrophy. Methods A mouse model of hypertrophy was established by Ang-II infusion through osmot- ic pump. And a cell model was also achieved based on Ang-Ⅱ-promoted hypertrophy in neonatal mouse ventricu- lar cardiomyocytes （NMVCs）. Enforced enhancement of miR-214-3p was obtained in a mouse Ang-II infusion model via tail vein injection of miR-214-3p agomir. Left-ventricular （LV） structure and function variables were assessed by transthoracic echocardiography. Wheat germ agglutinin （WGA） staining was used to show cell size of mouse myocardium eardiomyocytes. FITC- phalloidin staining was performed to show the cell area of NMVCs. Expressions of miR-214-3p, ANP and β-MHC were detected by real-time quantitative PCR and western -blot assay respectively. Results MiR-214-3p expression was markedly attenuated in hypertrophic myocardium of a mouse Ang-Ⅱ infusion model, but was increased in ang-Ⅱ-induced NMVCs. MiR-214-3p could significantly suppress the increase of cell size and protein expression of ANP and 1β-MHC in Ang-Ⅱ-treated NMVCs. Cardiac hypertrophy in a mouse Ang-Ⅱ infusion model was ameliorated by enforced increase of miR-214-3p, with the de- creases in cell size of cardiomyocyte and protein expression of ANP and β-MHC. Conclusion MiR-214-3p ex- pression is downregulated in the myocardium of a mouse Ang-Ⅱ infusion model, and miR-214-3p could suppress Ang-Ⅱ-induced cardiac hypertrophy.
Background Cardiac hypertrophy is an adaptive enlargement of the myocardium in response to stress or inju- ry. Many studies have revealed that microRNAs participate in cardiac hypertrophy, but the role of microRNA-214 -3p （miR-214-3p） in cardiac hypertrophy has not been illustrated. The present study aimed to investigate the ex- pression and potential role of miR-214-3p in a mouse model of angiotensin-II （Ang-II） infusion-induced myocar- dium hypertrophy. Methods A mouse model of hypertrophy was established by Ang-II infusion through osmot- ic pump. And a cell model was also achieved based on Ang-Ⅱ-promoted hypertrophy in neonatal mouse ventricu- lar cardiomyocytes （NMVCs）. Enforced enhancement of miR-214-3p was obtained in a mouse Ang-II infusion model via tail vein injection of miR-214-3p agomir. Left-ventricular （LV） structure and function variables were assessed by transthoracic echocardiography. Wheat germ agglutinin （WGA） staining was used to show cell size of mouse myocardium eardiomyocytes. FITC- phalloidin staining was performed to show the cell area of NMVCs. Expressions of miR-214-3p, ANP and β-MHC were detected by real-time quantitative PCR and western -blot assay respectively. Results MiR-214-3p expression was markedly attenuated in hypertrophic myocardium of a mouse Ang-Ⅱ infusion model, but was increased in ang-Ⅱ-induced NMVCs. MiR-214-3p could significantly suppress the increase of cell size and protein expression of ANP and 1β-MHC in Ang-Ⅱ-treated NMVCs. Cardiac hypertrophy in a mouse Ang-Ⅱ infusion model was ameliorated by enforced increase of miR-214-3p, with the de- creases in cell size of cardiomyocyte and protein expression of ANP and β-MHC. Conclusion MiR-214-3p ex- pression is downregulated in the myocardium of a mouse Ang-Ⅱ infusion model, and miR-214-3p could suppress Ang-Ⅱ-induced cardiac hypertrophy.
基金
supported by grants from the National Natural Science Foundation of China(No.81270222/81470439)
Natural Science Foundation of Guangdong Province(No.2014A030313635)
Translational Medicine Foundation of Guangdong General Hospital(No.2015zh06)
