MiR‐499 regulates myoblast proliferation and differentiation by targeting transforming growth factor β receptor 1

Wu, Jiyao; Yue, Binglin; Lan, Xianyong; Fang, Xingtang; Ma, Yun; Bai, Yueyu; Qi, Xingshan; Zhang, Chunlei

doi:10.1002/jcp.26903

Cited by 21 publications

(16 citation statements)

References 44 publications

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“…The present study demonstrated that miR-499-5p injection signi cantly decreased the diameter of muscle ber. The result was consistent with the previous studies because the diameter of slow-twitch muscle ber was smaller than fast-twitch muscle ber and miR-499-5p could regulate skeletal myo ber speci cation [9,15,19,20]. However, little is known about the metabolic change of miR-499-5p involvement in the process.…”

Section: Discussionsupporting

confidence: 92%

“…Recently, miRNAs have been shown to regulate gene expression and be involved in the proliferation and differentiation of skeletal muscle [18]. Previous evidence has indicated that miR-499-5p regulated skeletal myo ber speci cation by targeting Sox6 [15,19], Rod1 [19], Thrap1 [9], and TGFβR1 [20]. It was found in our previous study that miR-499-5p levels in skeletal muscle were decreased accompanied by increasing age.…”

Section: Discussionmentioning

confidence: 70%

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Sustained of mir-499-5p delivery from injection alters the muscle metabolomic profiles in broiler chicken

Li¹,

Lin²,

Yuan³

et al. 2020

Preprint

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Background Myogenic miRNAs (myomiRs) which dramatically increased during myogenesis have been shown to play critical roles in many aspects of muscle function. As a myomiR, miR-499-5p, has been identified to be highly expressed in cardiac and skeletal muscle. The study focused on the effects of miR-499-5p on muscle metabolism in broiler chicken. Methods In the current study, we assigned 16 broiler chicks to control group and treatment group and then monitored the effects using metabolomics. Chicks were fed basal diets without or with miR-499-5p delivery. Muscle samples were collected and analyzed by ultra-high-performance liquid chromatography–tandem mass spectrometry (UHPLC-MS/MS). Results Our findings revealed that miR-499-5p injection altered the concentrations of a variety of metabolites in the muscle. Thereinto, a total of 46 metabolites were identified at higher (P < 0.05) concentrations and 30 metabolites were identified at lower (P < 0.05) concentrations in the treatment group as compared with the control group. These metabolites were primarily involved with the regulation of lipid and carbohydrate metabolism. Further metabolic pathway analysis revealed that fructose and mannose metabolism, galactose metabolism, inositol phosphate metabolism and terpenoid backbone biosynthesis were the most important and critical pathway which may partially interpret the effects of miR-499-5p. Conclusions To our knowledge, this research is the first report of metabolic signatures and related metabolic pathways in the skeletal muscle for miR-499-5p injection and provide new insight into the effect of miRNA on growth performance.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 70%

Sustained of mir-499-5p delivery from injection alters the muscle metabolomic profiles in broiler chicken

Li¹,

Lin²,

Yuan³

et al. 2020

Preprint

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“…The targeted knockout of TAK1 caused increased oxidative stress and dysfunctional regeneration in response to muscle injury 14 . By contrast, many studies have shown that TAK1 activators inhibit myogenic differentiation, 42–44 implying that TAK1 is a negative regulator of differentiation. Moreover, other studies have indicated that TAK1 overexpression can increase proliferation and reduce differentiation 23,39 .…”

Section: Discussionmentioning

confidence: 99%

A potential therapeutic effect of catalpol in Duchenne muscular dystrophy revealed by binding with TAK1

Zhao

Jiang

et al. 2020

J cachexia sarcopenia muscle

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Background Duchenne muscular dystrophy (DMD) is a progressive muscle disease caused by the loss of dystrophin, which results in inflammation, fibrosis, and the inhibition of myoblast differentiation in skeletal muscle. Catalpol, an iridoid glycoside, improves skeletal muscle function by enhancing myogenesis; it has potential to treat DMD. We demonstrate the positive effects of catalpol in dystrophic skeletal muscle. Methods mdx (loss of dystrophin) mice (n = 18 per group) were treated with catalpol (200 mg/kg) for six consecutive weeks. Serum analysis, skeletal muscle performance and histology, muscle contractile function, and gene and protein expression were performed. Molecular docking and ligand-target interactions, RNA interference, immunofluorescence, and plasmids transfection were utilized to explore the protective mechanism in DMD by which catalpol binding with transforming growth factor-βactivated kinase 1 (TAK1) in skeletal muscle. Results Six weeks of catalpol treatment improved whole-body muscle health in mdx mice, which was characterized by reduced plasma creatine kinase (n = 18, À35.1%, P < 0.05) and lactic dehydrogenase (n = 18, À10.3%, P < 0.05) activity. These effects were accompanied by enhanced grip strength (n = 18, +25.4%, P < 0.05) and reduced fibrosis (n = 18, À29.0% for hydroxyproline content, P < 0.05). Moreover, catalpol treatment protected against muscle fatigue and promoted muscle recovery in the tibialis anterior (TA) and diaphragm (DIA) muscles (n = 6, +69.8%, P < 0.05 and + 74.8%, P < 0.001, respectively), which was accompanied by enhanced differentiation in primary myoblasts from DMD patients (n = 6, male, mean age: 4.7 ± 1.9 years) and mdx mice. In addition, catalpol eliminated p-TAK1 overexpression in mdx mice (n = 12, À21.3%, P < 0.05) and primary myoblasts. The catalpol-induced reduction in fibrosis and increased myoblast differentiation resulted from the inhibition of TAK1 phosphorylation, leading to reduced myoblast trans-differentiation into myofibroblasts. Catalpol inhibited the phosphorylation of TAK1 by binding to TAK1, possibly at Asp-206, Thr-208, Asn-211, Glu-297, Lys-294, and Tyr-293. Conclusions Our findings show that catalpol and TAK1 inhibitors substantially improve whole-body muscle health and the function of dystrophic skeletal muscles and may provide a novel therapy for DMD.

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“…Furthermore, selected miRNAs have been demonstrated to inhibit the myogenic differentiation acting on TGFβ and Wnt/β-catenin signaling. The myomiR miR-499 may inhibit TGFβ-receptor 1, promoting the proliferation of C2C12 cells [87], whereas miR-216a targets Smad7, a member of the inhibitory Smads family that can specifically inhibit TGFβ pathway and bovine primary muscle cells differentiation [88]. Inhibition of cell self-renewal progression of muscle precursors in the myogenic lineage has been attributed to miR-143-3p and miR-664-5p that downregulate Wnt5a, LRP5, Axin2, β-catenin and Wnt1 expression [89,90].…”

Section: Mirnas Role In Myogenesismentioning

confidence: 99%

Regulation of microRNAs in Satellite Cell Renewal, Muscle Function, Sarcopenia and the Role of Exercise

Fochi

Giuriato

Simone

et al. 2020

IJMS

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Sarcopenia refers to a condition of progressive loss of skeletal muscle mass and function associated with a higher risk of falls and fractures in older adults. Musculoskeletal aging leads to reduced muscle mass and strength, affecting the quality of life in elderly people. In recent years, several studies contributed to improve the knowledge of the pathophysiological alterations that lead to skeletal muscle dysfunction; however, the molecular mechanisms underlying sarcopenia are still not fully understood. Muscle development and homeostasis require a fine gene expression modulation by mechanisms in which microRNAs (miRNAs) play a crucial role. miRNAs modulate key steps of skeletal myogenesis including satellite cells renewal, skeletal muscle plasticity, and regeneration. Here, we provide an overview of the general aspects of muscle regeneration and miRNAs role in skeletal mass homeostasis and plasticity with a special interest in their expression in sarcopenia and skeletal muscle adaptation to exercise in the elderly.

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MiR‐499 regulates myoblast proliferation and differentiation by targeting transforming growth factor β receptor 1

Cited by 21 publications

References 44 publications

Sustained of mir-499-5p delivery from injection alters the muscle metabolomic profiles in broiler chicken

Sustained of mir-499-5p delivery from injection alters the muscle metabolomic profiles in broiler chicken

A potential therapeutic effect of catalpol in Duchenne muscular dystrophy revealed by binding with TAK1

Regulation of microRNAs in Satellite Cell Renewal, Muscle Function, Sarcopenia and the Role of Exercise

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