Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 295, Issue 30, Pages 10212-10223Publisher
ELSEVIER
DOI: 10.1074/jbc.RA119.012263
Keywords
muscle regeneration; inflammation; miR-223-3p; macrophage; cytokines; epigenetics; muscle satellite stem cell; small noncoding RNA; cytokine; interleukin-6 (IL-6)
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Funding
- National Natural Science Foundation of China [81430050, 81790622, 81871758]
- Beijing Hospitals Authority Youth Programme [QML20190604]
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After injury, the coordinated balance of pro- and anti-inflammatory factors in the microenvironment contribute to skeletal muscle regeneration. However, the underlying molecular mechanisms regulating this balance remain incompletely understood. In this study, we examined the roles of microRNAs (miRNAs) in inflammation and muscle regeneration. miRNA-Seq transcriptome analysis of mouse skeletal muscle revealed that miR-223-3p is upregulated in the early stage of muscle regeneration after injury. miR-223-3p knockout resulted in increased inflammation, impaired muscle regeneration, and increased interstitial fibrosis. Mechanistically, we found that myeloid-derived miR-223-3p suppresses the target gene interleukin-6 (Il6), associated with the maintenance of the proinflammatory macrophage phenotype during injury. Administration of IL-6-neutralizing antibody in miR-223-3p-knockout muscle could rescue the impaired regeneration ability and reduce the fibrosis. Together, our results reveal that miR-223-3p improves muscle regeneration by regulating inflammation, indicating that miRNAs can participate in skeletal muscle regeneration by controlling the balance of pro- and anti-inflammatory factors in the skeletal muscle microenvironment.
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