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Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications

ABSTRACT: Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications

PROVIDER: PRJNA1047047 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27008557_1.fastq.gz	Fastqsanger.gz
	SRR27008557_2.fastq.gz	Fastqsanger.gz
	SRR27008558_1.fastq.gz	Fastqsanger.gz
	SRR27008558_2.fastq.gz	Fastqsanger.gz
	SRR27008559_1.fastq.gz	Fastqsanger.gz

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Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications[gastrocnemius]

Project description:Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications[gastrocnemius]

| PRJNA1047280 | ENA

Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications[BAT]

Project description:Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications[BAT]

| PRJNA1047281 | ENA

Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications[gastrocnemius]

Project description:Myostatin (MSTN) has been discovered as a critical regulator of muscle mass. Recently, there has been an increasing interest in its functions in metabolism. Here, we specific knocked out MSTN in brown adipose tissue (BAT) (MSTNΔUCP1), and found that the MSTNΔUCP1 mice gained more weight than controls on high-fat diet, with progressive hepatosteatosis, and impaired skeletal muscle activity. RNA-seq analysis indicated signatures of mitochondrial dysfunction and inflammation in MSTN-ablation BAT. Further studies demonstrated that KLF4 is required for the metabolic phenotypes and FGF21 contributes to the microenvironment communication between adipocytes and macrophages induced by loss of MSTN in BAT. Moreover, MSTN-SMAD2/3-p38 signaling pathway mediated the expression of KLF4 and FGF21 in adipocytes. Taken together, brown adipocytes-derived MSTN governs metabolic niche in BAT and regulates systemic energy homeostasis.

2024-07-23 | GSE249029 | GEO

Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications[BAT]

2024-07-23 | GSE249028 | GEO

Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-07-23 | GSE249030 | GEO

Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communication.

Project description:Myostatin (MSTN) has long been recognized as a critical regulator of muscle mass. Recently, there has been increasing interest in its role in metabolism. In our study, we specifically knocked out MSTN in brown adipose tissue (BAT) from mice (MSTNΔUCP1) and found that the mice gained more weight than did controls when fed a high-fat diet, with progressive hepatosteatosis and impaired skeletal muscle activity. RNA-Seq analysis indicated signatures of mitochondrial dysfunction and inflammation in the MSTN-ablated BAT. Further studies demonstrated that Kruppel-like factor 4 (KLF4) was responsible for the metabolic phenotypes observed, whereas fibroblast growth factor 21 (FGF21) contributed to the microenvironment communication between adipocytes and macrophages induced by the loss of MSTN. Moreover, the MSTN/SMAD2/3-p38 signaling pathway mediated the expression of KLF4 and FGF21 in adipocytes. In summary, our findings suggest that brown adipocyte-derived MSTN regulated BAT thermogenesis via autocrine and paracrine effects on adipocytes or macrophages, ultimately regulating systemic energy homeostasis.

| S-EPMC11324308 | biostudies-literature

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

Project description: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.

2023-06-08 | MTBLS3345 | MetaboLights

PyMINEr Finds Gene and Autocrine/Paracrine Networks from Human Islet scRNAseq

Project description:Toolsets available for in-depth analysis of scRNAseq datasets by biologists with little informatics experience is limited. Here we describe an informatics tool (PyMINEr) that fully automates cell type identification, cell type-specific pathway analyses, graph theory-based analysis of gene regulation, and detection of autocrine/paracrine signaling networks in silico. We applied PyMINEr to interrogate human pancreatic islet scRNAseq datasets and discovered several features of co-expression graphs including: concordance of scRNAseq-graph structure with both protein-protein interactions and 3D-genomic architecture; association of high connectivity and low expression genes with cell type-enrichment; and potential for graph-structure to clarify potential etiologies of enigmatic disease-associated variants. We further created a consensus co-expression network and autocrine/paracrine signaling networks within and across islet cell types from 7-datasets. PyMINEr correctly identified changes in BMP/WNT signaling associated with cystic fibrosis pancreatic acinar-cell loss. This proof-of-principle study demonstrates that the PyMINEr framework will be a valuable resource for scRNAseq analyses.

2019-01-11 | GSE116753 | GEO

PyMINEr Finds Gene and Autocrine/Paracrine Networks from Human Islet scRNAseq

Project description:PyMINEr Finds Gene and Autocrine/Paracrine Networks from Human Islet scRNAseq

| PRJNA480045 | ENA

Skeletal muscle gene expression after myostatin knockout in mature mice

Project description:RNA from 5 mice with postdevelopmental knockout of myostatin and 5 mice with normal myostatin expression was analyzed with comprehensive oligonucleotide microarrays. Myostatin depletion affected the expression of several hundred genes at nominal P < 0.01, but fewer than a hundred effects were statistically significant according to a more stringent criterion (false discovery rate < 5%). Most of the effects were less than 1.5-fold in magnitude. In contrast to previously-reported effects of constitutive myostatin knockout, postdevelopmental knockout did not downregulate expression of genes encoding slow isoforms of contractile proteins or genes encoding proteins involved in energy metabolism. Several collagen genes were expressed at lower levels in the myostatin-deficient muscles, and this led to reduced tissue collagen levels as reflected by hydroxyproline content. Myostatin knockout tended to down-regulate the expression of sets of genes with promoter motifs for Smad3, Smad4, myogenin, NF-κB, serum response factor, and numerous other transcription factors. Main conclusions: in mature muscle, myostatin is a key transcriptional regulator of collagen genes, but not genes encoding contractile proteins or genes encoding proteins involved in energy metabolism.

2009-03-24 | GSE15349 | GEO

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