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Mir-24 Regulates Junctophilin-2 Expression in Cardiomyocytes
Ming Xu*, Hao-Di Wu*, Rong-Chang Li*, Hai-Bo Zhang*, Meng Wang*, Jin Tao, Xin-Heng Feng, Yun-Bo Guo, Su-Fang Li, Shao-Ting Lai, Peng Zhou, Lin-Lin Li, Hua-Qian Yang, Guan-Zheng Luo, Yan Bai, Jianzhong J. Xi, Wei Gao, Qi-De Han, You-Yi Zhang, Xiu-Jie Wang, Xu Meng, Shi-Qiang Wang
Rationale: Failing cardiomyocytes exhibit decreased efficiency of excitation-contraction (E-C) coupling. The downregulation of junctophilin-2 (JP2), a protein anchoring the sarcoplasmic reticulum to T-tubules, has been identified as a major mechanism underlying the defective E-C coupling. However, the regulatory mechanism of JP2 remains unknown. Objective: To determine whether microRNAs regulate JP2 expression. Methods and Results: Bioinformatic analysis predicted 2 potential binding sites of miR-24 in the 3′-untranslated regions of JP2 mRNA. Luciferase assays confirmed that miR-24 suppressed JP2 expression by binding to either of these sites. In the aortic stenosis model, miR-24 was upregulated in failing cardiomyocytes. Adenovirus-directed overexpression of miR-24 in cardiomyocytes decreased JP2 expression and reduced Ca2+ transient amplitude and E-C coupling gain. Conclusions: MiR-24–mediated suppression of JP2 expression provides a novel molecular mechanism for E-C coupling regulation in heart cells and suggests a new target against heart failure.
