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The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs (miRNA-seq)

ABSTRACT: Myostatin (MSTN) is a member of the TGF-β superfamily that negatively regulates skeletal muscle growth and differentiation. However, the mechanism by which complete MSTN deletion limits excessive proliferation of muscle cells remains unclear. In this study, we knocked out MSTN in mouse myoblast lines using a Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR/Cas9) system and sequenced the mRNA and miRNA transcriptomes. Our study suggests that complete loss of MSTN may limit excessive cell proliferation via activation of miRNAs.

ORGANISM(S): Mus musculus

PROVIDER: GSE124194 | GEO | 2018/12/21

REPOSITORIES: GEO

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The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs (mRNA-seq)

Project description:Myostatin (MSTN) is a member of the TGF-β superfamily that negatively regulates skeletal muscle growth and differentiation. However, the mechanism by which complete MSTN deletion limits excessive proliferation of muscle cells remains unclear. In this study, we knocked out MSTN in mouse myoblast lines using a Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR/Cas9) system and sequenced the mRNA and miRNA transcriptomes. Our study suggests that complete loss of MSTN may limit excessive cell proliferation via activation of miRNAs.

2018-12-21 | GSE124195 | GEO

Adult cardiomyocyte specific loss of myostatin

Project description:Inhibition of myostatin signaling induces strong skeletal muscle growth making it an attractive target to treat muscle wasting and sarcopenia. However, the biological function of myostatin in the heart is barely understood. We demonstrate that conditional inactivation of myostatin in the adult murine heart leads to cardiac hypertrophy, heart failure and increased lethality. To induce cardiomyocyte specific loss of myostatin a conditionally active Mstn^fl/fl allele was generated by insertion of loxP elements upstream and downstream of exons 1 and 2 of the mouse myostatin gene. The selection cassette was removed in vivo by flp-recombination. To inactivate myostatin, mice were mated to alphaMyHC-MCM mice (Sohal, DS, et al. (2001) Circulation Research 89, 20-25). Cre-recombination was achieved by intraperitoneal administration of Tamoxifen (40 mg/kg) for 5 consecutive days. The respective control alphaMyHC-MCM animals were equally treated.

2014-05-16 | E-MEXP-3744 | biostudies-arrayexpress

Gene co-expression network analysis of myostatin regulation at three different mouse developmental timepoints

Project description:Myostatin (Mstn) knockout mice exhibit large increases in skeletal muscle mass. However, relatively few of the genes that mediate or modify MSTN effects are known. In this study, we performed co-expression network analysis using whole transcriptome microarray data from Mstn-null and wild-type mice to identify genes involved in important biological processes and pathways related to skeletal muscle and adipose development.Genes differentially expressed between wild-type and Mstn-null mice were identified at 13.5 d.p.c. and 35 days after birth (d35) and further analyzed for shared DNA motifs using DREME. Known and novel transcription factor binding sites involved in MSTN signal transduction were enriched in differentially expressed genes. The use of regulatory impact factor (RIF), phenotypic impact factor (PIF), and differential hubbing analyses with the partical correlation and information theory (PCIT) co-expression analysis methods identified both known and potentially novel regulators of muscle development. These results provide new details of how MSTN may mediate transcriptional regulation as well as insight into novel regulators of MSTN signal transduction that merit further study regarding their physiological roles in muscle and adipose development.

2014-11-11 | GSE63154 | GEO

Myostatin Increases Trophoblast Cell Invasion Through Regulating Epithelial Mesenchymal Transition Genes

Project description:Myostatin (MSTN) is a TGF-β superfamily member and was recently shown to be secreted and functioning in the placenta. In this study, we perfomed mRNA sequencing on control and MSTN-treated primary trophoblast cells to decipher the underlying molecular mechanisms involved in MSTN-induced human trophoblast cell invasion.

2023-02-18 | GSE225378 | GEO

Myostatin Deficiency But Not Anti-Myostatin Blockade Induces Marked Proteomic Changes in Mouse Skeletal Muscle

Project description:Recent studies have reported the deleterious physiological and metabolic changes in Mstn-/- mice including impaired force generation and susceptibility to contraction-induced injury. Such observations have raised the concerns about the functional quality of the increased muscle resulting from therapeutic blockade of Mstn. Here we provide proteomic evidence to demonstrate that therapeutic Mstn inhibition has minimal effects on muscle proteome composition whereas the genetic ablation of Mstn induces marked changes. Furthermore, this study also represents the first proteomic analysis of the pharmacological blockage of the Mstn/activin receptor pathway being actively pursued as a potential therapy for multiple muscle wasting disorders.

2016-05-31 | PXD003747 | Pride

Effect of Genetically Reduced Maternal Myostatin on Late Gestation Maternal, Fetal, and Placental Metabolomes in Mice

Project description:<p>Myostatin (gene symbol: Mstn) is an autocrine and paracrine inhibitor of muscle growth. Pregnant mice with genetically reduced levels of myostatin give birth to offspring with greater adult muscle mass and bone biomechanical strength. However, maternal myostatin is not detectable in fetal circulations. Fetal growth is dependent on the maternal environment, and the provisioning of nutrients and growth factors by the placenta. Thus, this study examined the effect of reduced maternal myostatin on maternal and fetal serum metabolomes, as well as the placental metabolome. Fetal and maternal serum metabolomes were highly distinct, which is consistent with the role of the placenta in creating a specific fetal nutrient environment. There was no effect from myostatin on maternal glucose tolerance or fasting insulin. In comparisons between pregnant control and Mstn+/− mice, there were more significantly different metabolite concentrations in fetal serum, at 50, than in the mother’s serum at 33, confirming the effect of maternal myostatin reduction on the fetal metabolic milieu. Polyamines, lysophospholipids, fatty acid oxidation, and vitamin C, in fetal serum, were all affected by maternal myostatin reduction.</p>

2023-06-08 | MTBLS3345 | MetaboLights

The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs

Project description:The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs

| PRJNA510976 | ENA

The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs (miRNA-seq)

Project description:The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs (miRNA-seq)

| PRJNA510977 | ENA

The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs (mRNA-seq)

Project description:The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs (mRNA-seq)

| PRJNA510980 | ENA

Muscle Hypertrophy Induced by Myostatin Inhibition Accelerates Degeneration in Dysferlinopathy

Project description:Because myostatin normally limits skeletal muscle growth, there is an extensive effort to develop myostatin inhibitors for clinical use. One potential concern is that in patients with muscle degenerative diseases, inducing hypertrophy may increase stress on dystrophic fibers. Here, we show that blocking the myostatin pathway in dysferlin mutant mice results in early improvement in histopathology but ultimately accelerates muscle degeneration. Hence, benefits of this approach should be weighed against these potential detrimental effects.

2015-09-04 | GSE62945 | GEO

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