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Updated: Feb 8, 2026

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart
Published on: June 14, 2020
mir-127-3p inhibits the proliferation of myocytes by targeting KMT5a
Renqiang Yuan1, Xumeng Zhang1, Ying Fang1
1State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
Abstract:
MicroRNAs are a class of highly conserved ∼20 nucleotides non-coding RNAs that post-transcriptionally regulate gene expression. Many miRNAs were studied in the development of skeletal muscle, such as miR-1, miR-206, and miR-133. In our previous study, miR-127-3p was found highly expressed in porcine fetal skeletal muscle, whereas the detailed functions of miR-127-3p in muscle development is still unclear. In this study, we detected that miR-127-3p also highly expressed in skeletal muscle, cardiac muscle of adult mice and proliferative C2C12 cell lines. Overexpression of miR-127-3p almost has no effects on differentiation of C2C12 cell lines. However, miR-127-3p significantly inhibited the cell proliferation of C2C12 cells. Moreover, we identified KMT5a as a target gene that was down-regulated in both mRNA and protein level when miR-127-3p mimics were introduced. Furthermore, KMT5a overexpression in miR-127-3p treated cells rescued the influence of miR-127-3p on C2C12 proliferation. In brief, our data reveals that miR-127-3p regulates the proliferation of myocytes through KMT5a.
Insights
MicroRNAs regulate gene expression. This study shows microRNA-127-3p inhibits myocyte proliferation by down-regulating KMT5a, revealing a novel mechanism in muscle development.
Area of Science:
- Molecular Biology
- Gene Regulation
- Muscle Development
Background:
- MicroRNAs (miRNAs) are key post-transcriptional regulators of gene expression.
- While several miRNAs are known to influence skeletal muscle development, the role of miR-127-3p remains largely uncharacterized.
- Previous studies indicated high expression of miR-127-3p in porcine fetal skeletal muscle.
Purpose of the Study:
- To investigate the function of miR-127-3p in muscle cell proliferation and differentiation.
- To identify the molecular targets and mechanisms underlying miR-127-3p's role in myocytes.
Main Methods:
- Quantification of miR-127-3p expression in mouse skeletal and cardiac muscle, and C2C12 cell lines.
- Overexpression of miR-127-3p in C2C12 cells to assess effects on proliferation and differentiation.
- Identification and validation of KMT5a as a direct target gene using mRNA and protein analysis.
- Rescue experiments involving KMT5a overexpression in miR-127-3p treated cells.
Main Results:
- miR-127-3p was highly expressed in adult mouse skeletal and cardiac muscle, and proliferating C2C12 cells.
- Overexpression of miR-127-3p significantly inhibited C2C12 cell proliferation but did not affect differentiation.
- KMT5a was identified as a direct target, with its mRNA and protein levels reduced by miR-127-3p.
- KMT5a re-expression rescued the inhibitory effect of miR-127-3p on C2C12 cell proliferation.
Conclusions:
- miR-127-3p plays a significant role in regulating myocyte proliferation.
- The mechanism involves the down-regulation of its target gene, KMT5a.
- This study elucidates a novel function of miR-127-3p in muscle cell biology.
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