Zfp422 promotes skeletal muscle differentiation by regulating EphA7 to induce appropriate myoblast apoptosis

Nie, Yaping; Cai, Shaohui; Yuan, Renqiang; Ding, Suying; Zhang, Xumeng; Chen, Luxi; Chen, Yaosheng; Mo, Delin

doi:10.1038/s41418-019-0448-9

Cited by 18 publications

(11 citation statements)

References 57 publications

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“…In addition, accompanied by impaired myogenic differentiation in SelK KO mice and siSelK C2C12 myoblasts, excessive autophagy and apoptosis were identified in our study. Autophagy and apoptosis coexist in early muscle injury throughout regeneration because the former is responsible for cell reprogramming by regulating cytoplasmic remodelling, while the latter eliminates defective cells that do not have differentiation potential [ 49 , 50 ]. The crosstalk between apoptosis and autophagy determines the balance of cell survival and death, allowing SCs to differentiate normally [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

et al. 2022

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Section: Discussionmentioning

confidence: 99%

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

et al. 2022

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“…In terms of gene expression, Zn can be a mediator on DNA and RNA transcription by the formation of Zn-finger proteins ( ZNF ), which are required for interaction with DNA, RNA, and other proteins, leading to the regulation of cellular processes ( Hostetler et al, 2003 ; Cassandri et al, 2017 ). Previous studies showed that ZNF play a critical role in myogenic synthesis and differentiation with recruiting muscle-specific target genes ( Cassandri et al, 2017 ; Nie et al, 2019 ). Salmon et al (2009) showed that overexpression of ZNF could promote myogenic proliferation and inhibit differentiation.…”

Section: Discussionmentioning

confidence: 99%

Effects of mineral methionine hydroxy analog chelate in sow diets on epigenetic modification and growth of progeny

Jang

Kim

Purvis³

et al. 2020

Journal of Animal Science

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The study was conducted to determine the effects of mineral methionine hydroxy analogue chelate (MMHAC) partially replacing inorganic trace minerals in sow diets on epigenetic and transcriptional changes in muscle and jejunum of progeny. The MMHAC is zinc (Zn), manganese (Mn), and copper (Cu) chelated with methionine hydroxy analogue (Zn-, Mn-, and Cu-MHAC). On d 35 of gestation, 60 pregnant sows were allotted to 2 dietary treatments in a randomized completed block design using parity as a block: (1) ITM: inorganic trace minerals with zinc sulfate (ZnSO4), manganese oxide (MnO), and copper sulfate (CuSO4) and (2) CTM: 50% of ITM was replaced with MMHAC (MINTREXtrace minerals, Novus International Inc., St Charles, MO). Gestation and lactation diets were formulated to meet or exceed NRC requirements. On d 1 and 18 of lactation, milk samples from 16 sows per treatment were collected to measure immunoglobulins (IgG, IgA, and IgM) and micromineral concentrations. Two pigs per litter were selected to collect blood to measure the concentration of immunoglobulins in the serum, and then euthanized to collect jejunal mucosa, jejunum tissues, and longissimus muscle to measure global DNA methylation, histone acetylation, cytokines, and jejunal histomorphology at birth and d 18 of lactation. Data were analyzed using Proc MIXED of SAS. Supplementation of MMHAC tended to decrease (P = 0.059) body weight (BW) loss of sows during lactation and tended to increase (P = 0.098) piglet BW on d 18 of lactation. Supplementation of MMHAC increased (P < 0.05) global histone acetylation and tended to decrease myogenic regulatory factor 4 (MRF4) messenger ribonucleic acid (mRNA) (P = 0.068) and delta 4-desaturase sphingolipid1 (DEGS1) mRNA (P = 0.086) in longissimus muscle of piglets at birth. Supplementation of MMHAC decreased (P < 0.05) nuclear factor kappa B (NF-κB) mRNA in the jejunum and DEGS1 mRNA in longissimus muscle, and tended to decrease mucin-2 (MUC2) mRNA (P = 0.057) and transforming growth factor beta 1 (TGF-β1) mRNA (P = 0.057) in the jejunum of piglets on d 18 of lactation. There were, however, no changes in the amounts of TNF-α, IL-8, TGF-β, MUC2, and MYF6 in the tissues by MMHAC. In conclusion, maternal supplementation of MMHAC could contribute to histone acetylation and programming in the fetus, which potentially regulates intestinal health and skeletal muscle development of piglets at birth and weaning, possibly leading to enhanced growth of their piglets.

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“…DAPI was used to visualize cell nuclei with a fluorescence microscope (DP80; Olympus, Japan). The differentiation index was calculated as the percentage of nuclei in MyHC positive cells, and the fusion index was calculated as the percentage of nuclei in fused myotubes which have two or more nuclei out of the total nuclei 35 …”

Section: Methodsmentioning

confidence: 99%

lncMGPF is a novel positive regulator of muscle growth and regeneration

Jin

et al. 2020

J cachexia sarcopenia muscle

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Background Long non-coding RNAs (lncRNAs) play critical regulatory roles in diverse biological processes and diseases. While a large number of lncRNAs have been identified in skeletal muscles until now, their function and underlying mechanisms in skeletal myogenesis remain largely unclear. Methods We characterized a novel functional lncRNA designated lncMGPF (lncRNA muscle growth promoting factor) using RACE, Northern blot, fluorescence in situ hybridization and quantitative real-time PCR. Its function was determined by gene overexpression, interference, and knockout experiments in C2C12 myoblasts, myogenic progenitor cells, and an animal model. The molecular mechanism by which lncMGPF regulates muscle differentiation was mainly examined by cotransfection experiments, luciferase reporter assay, RNA immunoprecipitation, RNA pull-down, and RNA stability analyses. Results We report that lncMGPF, which is highly expressed in muscles and positively regulated by myoblast determination factor (MyoD), promotes myogenic differentiation of muscle cells in vivo and in vitro. lncMGPF knockout in mice substantially decreases growth rate, reduces muscle mass, and impairs muscle regeneration. Overexpression of lncMGPF in muscles can rescue the muscle phenotype of knockout mice and promote muscle growth of wild-type mice. Mechanistically, lncMGPF promotes muscle differentiation by acting as a molecular sponge of miR-135a-5p and thus increasing the expression of myocyte enhancer factor 2C (MEF2C), as well as by enhancing human antigen R-mediated messenger RNA stabilization of myogenic regulatory genes such as MyoD and myogenin (MyoG). We confirm that pig lncRNA AK394747 and human lncRNA MT510647 are homologous to mouse lncMGPF, with conserved function and mechanism during myogenesis. Conclusions Our data reveal that lncMGPF is a novel positive regulator of myogenic differentiation, muscle growth and regeneration in mice, pigs, and humans.

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Zfp422 promotes skeletal muscle differentiation by regulating EphA7 to induce appropriate myoblast apoptosis

Cited by 18 publications

References 57 publications

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

Effects of mineral methionine hydroxy analog chelate in sow diets on epigenetic modification and growth of progeny

lncMGPF is a novel positive regulator of muscle growth and regeneration

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