Astragalus polysaccharide mediates lnc-GD2H to regulate proliferation and differentiation of C2C12 muscle cells under hypoxic condition.

Astragalus polysaccharide (APS) is a bioactive component of Astragalus species that shows protective effects on C2C12 muscle cell proliferation and differentiation under hypoxic conditions. In this study, EdU staining, cell scratch testing, quantitative reverse-transcription polymerase chain reaction, Western blotting, immunofluorescence analysis, and lnc-GD2H silencing were used to investigated the protective effects and mechanisms of action of APS against CoCl-induced hypoxic injury of muscle cells. Our results showed that APS promoted cell proliferation and increased the expression of lnc-GD2H, c-Myc, and Ki-67.

Running improves muscle mass by activating autophagic flux and inhibiting ubiquitination degradation in mdx mice.

Background: Exercise therapy can improve muscle mass, strengthen muscle and cardiorespiratory function, and may be an excellent adjunctive treatment option for Duchenne muscular dystrophy.

Methods: This article investigates the effects of 10 weeks of treadmill training on skeletal muscle in control and mdx mice. Hematoxylin and eosin (H&E) staining was used to detect the morphometry of skeletal muscle; the grip strength test, suspension test, and rotarod test were used to detect limb muscle strength of mice, and Aurora Scientific Instruments were used to detect in vivo Muscle Stimulation Measuring Maximum Force of pre-fatigue and post-fatigue.

Roles of super enhancers and enhancer RNAs in skeletal muscle development and disease.

Skeletal muscle development is a multistep biological process regulated by a variety of myogenic regulatory factors, including MyoG, MyoD, Myf5, and Myf6 (also known as MRF4), as well as members of the FoxO subfamily. Differentiation and regeneration during skeletal muscle myogenesis contribute to the physiological function of muscles. Super enhancers (SEs) and enhancer RNAs (eRNAs) are involved in the regulation of development and diseases.

Nec-1 alleviated the deleterious effect of CoCl on C2C12 myoblast differentiation and fusion via the mTOR pathway.

Myoblast differentiation and fusion are vital for muscle development and repair in mammals. We previously showed that necrostatin-1(Nec-1) protects C2C12 myotubes from cobalt chloride (CoCl)-induced pseudo-hypoxia. However, the function of Nec-1 in mouse C2C12 myoblast differentiation and fusion was still unknown.

[Effects of Atrolnc-1 on immobilization induced muscular atrophy in mice hindlimbs].

To investigate the effects of Atrolnc-1 on immobilization induced muscular atrophy in mice hindlimbs. Male C57BL/6 mice were randomly divided into control group and immobilization group (=10 per group). The control group did not receive any treatment.

Lnc-GD2H Promotes Proliferation by Forming a Feedback Loop With c-Myc and Enhances Differentiation Through Interacting With NACA to Upregulate Myog in C2C12 Myoblasts.

In the present study, the roles of a novel long non-coding RNA (lncRNA), lnc-GD2H, in promoting C2C12 myoblast proliferation and differentiation and muscle regeneration were investigated by quantitative polymerase chain reaction, western blotting, Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine (EdU), immunofluorescence staining, luciferase reporter, mass spectrometry, pulldown, chromatin immunoprecipitation, RNA immunoprecipitation assay, wound healing assays, and cardiotoxin (CTX)-induced muscle injury assays. It was observed that lnc-GD2H promoted myoblast proliferation as evidenced by the enhancement of the proliferation markers c-Myc, CDK2, CDK4, and CDK6, percentage of EdU-positive cells, and rate of cell survival during C2C12 myoblast proliferation. Additional experiments confirmed that c-Myc bound to the lnc-GD2H promoter and regulated its transcription.

Knockdown of CNN3 Impairs Myoblast Proliferation, Differentiation, and Protein Synthesis via the mTOR Pathway.

Background: Myogenesis is a complex process that requires optimal outside-in substrate-cell signaling. Calponin 3 (CNN3) plays an important role in regulating myogenic differentiation and muscle regeneration; however, the precise function of CNN3 in myogenesis regulation remains poorly understood. Here, we investigated the role of CNN3 in a knockdown model in the mouse muscle cell line C2C12.

Role of miRNAs and lncRNAs in dexamethasone-induced myotube atrophy .

Skeletal muscle atrophy is a well-known adverse effect of long-term glucocorticoid (GC) therapy. MicroRNAs (miRNAs or miRs) and long non-coding RNAs (lncRNAs) are important regulators in a number of physiological and pathological processes. However, the role of miRNAs and lncRNAs in the regulation of GC-treated muscle atrophy remains poorly understood.

Regulation of Skeletal Muscle Atrophy in Cachexia by MicroRNAs and Long Non-coding RNAs.

Skeletal muscle atrophy is a common complication of cachexia, characterized by progressive bodyweight loss and decreased muscle strength, and it significantly increases the risks of morbidity and mortality in the population with atrophy. Numerous complications associated with decreased muscle function can activate catabolism, reduce anabolism, and impair muscle regeneration, leading to muscle wasting. microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), types of non-coding RNAs, are important for regulation of skeletal muscle development.

Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo.

Starvation or severe deprivation of nutrients, which is commonly seen in surgical patients, can result in catabolic changes in skeletal muscles, such as muscle atrophy. Therefore, it is important to elucidate the underlying molecular regulatory mechanisms during skeletal muscle atrophy. In the present study, muscular atrophy was induced by starvation and the results demonstrated that myosin heavy chain was decreased, whereas muscle RING finger protein 1 and atrogin‑1 were increased, both in vitro and in vivo.

Differentially expressed coding and noncoding RNAs in CoCl-induced cytotoxicity of C2C12 cells.

Aim: We aimed to explore potential regulators of coding and noncoding RNAs (ncRNAs) in Co(II) ion-induced myo cytotoxicity.

Materials & Methods: We confirmed the toxic effects of Co(II) on mouse skeletal C2C12 myotubes by CoCl, and performed the expression profiles of circular RNAs (circRNAs), long noncoding RNAs (lncRNAs) and mRNAs using microarray analysis. We constructed co-expression, competing endogenous RNA and cis/trans regulation networks for ncRNAs, and filtered 71 candidate circRNAs with coding potential.

Expression of circular RNAs during C2C12 myoblast differentiation and prediction of coding potential based on the number of open reading frames and N6-methyladenosine motifs.

The importance of circular RNAs (circRNAs) as regulators of muscle development and muscle-associated disorders is becoming increasingly apparent. To explore potential regulators of muscle differentiation, we determined the expression profiles of circRNAs of skeletal muscle C2C12 myoblasts and myotubes using microarray analysis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to explore circRNA functions.

Necrostatin-1 protects C2C12 myotubes from CoCl2-induced hypoxia.

Necrostatin-1 (Nec-1) is a selective and potent allosteric inhibitor of necroptosis by specifically inhibiting the activity of receptor‑interacting protein (RIP) 1 kinase. The aim of the present study was to determine the effect of Nec‑1 on an anoxia model comprising mouse skeletal C2C12 myotubes. In the present study, a hypoxic mimetic reagent, cobalt chloride (CoCl2), was used to induce hypoxia in C2C12 myotubes.

Effects of Cobalt Chloride, a Hypoxia-Mimetic Agent, on Autophagy and Atrophy in Skeletal C2C12 Myotubes.

Background: Hypoxia-induced autophagy and muscle wasting occur in several environmental and pathological conditions. However, the molecular mechanisms underlying the effects of the hypoxia-mimetic agent CoCl on autophagy and muscle atrophy are still unclear.

Methods: C2C12 myotubes were exposed to increasing concentrations of CoCl for 24 hours.