ArticleAmerican journal of physiology. Cell physiology2014
miR-23a is decreased during muscle atrophy by a mechanism that includes calcineurin signaling and exosome-mediated export.
Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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86 citing papers in PubMed, 130 citations in OpenAlex.
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- Small Extracellular Vesicle Release Following Electrical Pulse Stimulation of C2C12 Myotubes: Effects on microRNA Cargo and Myoblast Migration and Differentiation.International journal of molecular sciences · 2026Article
- The Role of Extracellular Vesicles MicroRNAs in Sarcopenia: From Aging to Multi-Morbidity.Aging medicine (Milton (N.S.W)) · 2026Review
- RNA cargo profiling of muscle extracellular vesicles identifies candidate biomarkers of disease activity and muscle degeneration in FSHD.Journal of translational medicine · 2026Article
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- Sphingolipids in Extracellular Vesicles Released From the Skeletal Muscle Plasma Membrane Control Muscle Stem Cell Fate During Muscle Regeneration.Journal of extracellular vesicles · 2025Article
- Extracellular Vesicles in Sport Horses: Potential Biomarkers and Modulators of Exercise Adaptation and Therapeutics.International journal of molecular sciences · 2025Review
- Comparative proteomics and micro-RNA analysis of skeletal muscle cell small extracellular vesicles - Unique profiles in cells from severely obese individuals with type 2 diabetesFrontiers in physiology · 2025Article
- Senescent renal tubular cells derived extracellular vesicles transported miR-20a and miR-21 induced macrophage-to-myofibroblast transition in renal fibrosis after ischemia reperfusion injury.International journal of biological sciences · 2025Article
- New perspectives of the role of skeletal muscle derived extracellular vesicles in the pathogenesis of amyotrophic lateral sclerosis: the 'dying back' hypothesis.Journal of extracellular biology · 2024Review
- MiR-126 accelerates renal injury induced by UUO via inhibition PI3K/ IRS-1/ FAK signaling induced M2 polarization and endocytosis in macrophages.Scientific reports · 2024Article
- Recent Advances of Exosomes Derived from Skeletal Muscle and Crosstalk with Other Tissues.International journal of molecular sciences · 2024Review
- Review
- Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024Review
- Muscle-derived extracellular vesicles mediate crosstalk between skeletal muscle and other organs.Frontiers in physiology · 2024Review
- Exercise-derived skeletal myogenic exosomes as mediators of intercellular crosstalk: a major player in health, disease, and exercise.Journal of physiology and biochemistry · 2023Review
- Plasma Exosomal microRNA Profile Reveals miRNA 148a-3p Downregulation in the Mucosal-Dominant Variant of Pemphigus Vulgaris.International journal of molecular sciences · 2023Article
26 more citing papers are in PubMed but not listed here.
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8 authors at 2 institutions in 1 country.
Funding
Abstract
Skeletal muscle atrophy is prevalent in chronic diseases, and microRNAs (miRs) may play a key role in the wasting process. miR-23a was previously shown to inhibit the expression of atrogin-1 and muscle RING-finger protein-1 (MuRF1) in muscle. It also was reported to be regulated by cytoplasmic nuclear factor of activated T cells 3 (NFATc3) in cardiomyocytes. The objective of this study was to determine if miR-23a is regulated during muscle atrophy and to evaluate the relationship between calcineurin (Cn)/NFAT signaling and miR-23a expression in skeletal muscle cells during atrophy. miR-23a was decreased in the gastrocnemius of rats with acute streptozotocin-induced diabetes, a condition known to increase atrogin-1 and MuRF1 expression and cause atrophy. Treatment of C2C12 myotubes with dexamethasone (Dex) for 48 h also reduced miR-23a as well as RCAN1.4 mRNA, which is transcriptionally regulated by NFAT. NFATc3 nuclear localization and the amount of miR-23a decreased rapidly within 1 h of Dex administration, suggesting a link between Cn signaling and miR-23a. The level of miR-23a was lower in primary myotubes from mice lacking the α- or β-isoform of the CnA catalytic subunit than wild-type mice. Dex did not further suppress miR-23a in myotubes from Cn-deficient mice. Overexpression of CnAβ in C2C12 myotubes prevented Dex-induced suppression of miR-23a. Finally, miR-23a was present in exosomes isolated from the media of C2C12 myotubes, and Dex increased its exosomal abundance. Dex did not alter the number of exosomes released into the media. We conclude that atrophy-inducing conditions downregulate miR-23a in muscle by mechanisms involving attenuated Cn/NFAT signaling and selective packaging into exosomes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.