Related Experiment Video
Updated: May 19, 2026

Visualization of Cell Cycle Variations and Determination of Nucleation in Postnatal Cardiomyocytes
Published on: February 24, 2017
Mir-24 regulates junctophilin-2 expression in cardiomyocytes
Ming Xu1, Hao-Di Wu, Rong-Chang Li
1State Key Laboratory of Biomembrane and Membrane Biotechnology, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Third Hospital, College of Engineering and College of Life Sciences, Peking University, China.
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 Ca(2+) 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.
Related Concept Videos
Cardiomyopathy IV: Restrictive Cardiomyopathy
Master Transcription Regulators
MAPK Signaling Cascades
