Affiliation:
1. Department of Cardiology 1st Affiliated Hospital of Anhui Medical University Hefei Anhui China
2. Department of Oncology, Hefei Cancer Hospital Chinese Academy of Sciences Hefei Anhui China
3. Department of Anatomy, The Research Center of Basic Integrative Medicine Guangzhou University of Traditional Chinese Medicine Guangzhou Guangdong China
Abstract
AbstractCardiac hypertrophy, worldwide known as an adaptive functional compensatory state of myocardial stress, is mainly believed to proceed to severe heart diseases, even to sudden death. Emerging studies have explored the microRNA alteration during hypertrophy. However, the mechanisms of microRNAs involved in cardiac hypertrophy are still uncertain. We studied young rats to establish abdominal aorta coarctation (AAC) for 4 weeks. With the significant downregulated cardiac function and upregulated hypertrophic biomarkers, AAC‐induced rats showed enlarged myocardiocytes and alterations in microRNAs, especially downregulated miR‐31‐5p. miR‐31‐5p targets the 3′UTR of Nfatc2ip and inhibits myocardial hypertrophy in vitro and in vivo. Furthermore, we verified that Nfatc2ip is necessary and sufficient for cardiac hypertrophy in neonatal rat cardiomyocytes. Moreover, we found miR‐31‐5p inhibited the colocalization of Nfatc2ip and hypertrophic gene β‐Mhc. Luciferase assay and ChiP‐qPCR test demonstrated that Nfatc2ip binded to the core‐promoter of β‐Mhc and enhanced its transcriptional activity. Above all, our study found a new pathway, mir‐31‐5p/Nfatc2ip/β‐Mhc, which is involved in cardiac hypertrophy, suggesting a potential target for intervention of cardiac hypertrophy.