GDF11 rapidly increases lipid accumulation in liver cancer cells through ALK5-dependent signaling
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ABSTRACT:
PROVIDER: PRJNA698228 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13588044.fastq.gz | Fastqsanger.gz | |||
| SRR13588045.fastq.gz | Fastqsanger.gz | |||
| SRR13588046.fastq.gz | Fastqsanger.gz | |||
| SRR13588047.fastq.gz | Fastqsanger.gz | |||
| SRR13588048.fastq.gz | Fastqsanger.gz |
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Project description:Here we used RNA-Seq to unravel the gene expression patterns and related signaling pathways that might be responsible for the observed changes in the lipidome upon GDF11 treatment of hepatocellular carcinoma cells (HCC), HepG2. RNA-seq analysis was performed after 24h of GDF11 (100ng/ml) treatment to investigate its involvement in lipid metabolism. Genes exhibiting absolute fold-change values >2 and p-values <0.05 were considered differentially expressed between contrasts and statistical differences in gene expression were assessed by the ANOVA test. The significance threshold was set to 0.05. Treatment with recombinant GDF11 had an extensive effect on the overall gene expression profile in HepG2 cells and heatmap analysis clearly segregated control and GDF11 treated samples. In total, we identified 3,357 differentially expressed genes, of which 2,422 were over-expressed, and 935 were downregulated. To gain more deep mechanistic insight into the biological processes and pathway associations with these differentially expressed genes, we analyzed our transcriptomic data by STRING pathway unbiased analysis for annotated molecular interactions of selected genes employing Kegg pathways database. The 5 top most significantly influenced canonical pathways/cellular processes were the ones related to TGF-β signaling, extracellular matrix remodeling, focal adhesion, PI3K-AKT signaling, and cytochrome P450-dependent metabolism.
2021-01-31 | GSE165842 | GEO
Project description:GDF11 treatment leads to bone loss in mice and strongly stimulates RANKL-induced osteoclastogenesis of bone marrow-derived macrophages (BMMs) in vitro. We used microarrays to identified distinct classes of up-regulated genes in BMMs after GDF11 treatment. Mouse BMMs were treated with or without GDF11 for RNA extraction and and hybridization on Affymetrix microarrays
2016-07-21 | E-GEOD-84609 | biostudies-arrayexpress
Project description:Age-related frailty may in part be due to a decreased competency in skeletal muscle regeneration. The role of the closely related TGFbeta amily molecules myostatin and GDF11 in regeneration is unclear. The commercially available antibody which in a prior report was used to demonstrate an age-related decrease in GDF11 was found to detect both GDF11 and myostatin, and with this reagent it appears that the combination of GDF11 and myostatin increases with age in serum. Mechanistically, GDF11 and myostatin induce SMAD2/3 phosphorylation, and both inhibit myoblast differentiation and regulate identical downstream signaling. GDF11 injected into adult mice in a model of regeneration induces an increase in smaller fibers and a decrease in satellite cell expansion. There are no signs of benefit from GDF11 to regeneration. Thus, GDF11 appears to be an age-associated myokine that inhibits muscle differentiation, and is thus a target for blockade to treat frailty
2015-05-20 | GSE67326 | GEO
Project description:Growth differentiation factor 11 (GDF11), is one of the members of transforming growth factor β (TGFβ) superfamily. We set out to unequivocally reveal the effect of endogenous GDF11 on biological process by adopting CRISPR/Cas9 gene knockout strategy to specifically delete GDF11 gene in Neuro-2a cells. We analyze mRNA profiles of differentially genes in wild type (WT) and GDF11 knockout (GDF11-/-) Neuro-2a cells by using RNA-seq technology. The RNA-seq data reported here provide a fundamental materials and evidence for investigations of biological function of GDF11.
2021-10-06 | GSE167538 | GEO
Project description:GDF11 treatment leads to bone loss in mice and strongly stimulates RANKL-induced osteoclastogenesis of bone marrow–derived macrophages (BMMs) in vitro. We used microarrays to identified distinct classes of up-regulated genes in BMMs after GDF11 treatment.
2016-07-21 | GSE84609 | GEO
Project description:In this study, we investigated signaling pathways in Skeletal muscle precursors that are altered with aging and age-related deficits in muscle regenerative potential. We performed fluorescence activated cell sorting (FACS) to obtain highly purified skeletal muscle satellite cells from young, middle-aged and old mice. Parabiosis experiments indicate that impaired regeneration in aged mice is reversible by exposure to a young circulation, suggesting that young blood contains humoral "rejuvenating" factors that can restore regenerative function. Here, we demonstrate that the circulating protein growth differentiation factor 11 (GDF11) is a rejuvenating factor for skeletal muscle. Supplementation of systemic GDF11 levels, which normally decline with age, by heterochronic parabiosis or systemic delivery of recombinant protein, reversed functional impairments and restored genomic integrity in aged muscle stem cells (satellite cells). Increased GDF11 levels in aged mice also improved muscle structural and functional features and increased strength and endurance exercise capacity. These data indicate that GDF11 systemically regulates muscle aging and may be therapeutically useful for reversing age-related skeletal muscle and stem cell dysfunction. We used Affymetrix Mouse Genome array to identify global transcriptional changes associated with age in skeletal muscle precursors.
2014-05-08 | E-GEOD-50821 | biostudies-arrayexpress
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tissue-tissue interactions between myogenic precursors of craniofacial muscles and cranial neural crest cells (CNCCs). Here, we conducted gene expression profiling of the tongue bud from mice at embryonic day E13.5 with a CNCC-specific conditional inactivation of the TGF-beta receptor type 1 gene Alk5. These mice provide a model of microglossia as well as disrupted extraocular and masticatory muscle development, which are congenital birth defects commonly observed in several syndromic conditions. To investigate the adverse effects of dysfunctional TGF-beta signaling on tissue-tissue interactions between CNCCs and myogenic precursors of craniofacial muscles, we analyzed tongue bud tissue of mice with a CNCC-specific conditional inactivation of Alk5 (Wnt1-Cre; Alk5 fl/fl). We performed microarray analyses of the tongue bud of Alk5 fl/fl control mice and Wnt1-Cre; Alk5 fl/fl mutant mice, collected at embryonic day E13.5 (n=4 per group).
2014-06-18 | E-GEOD-52358 | biostudies-arrayexpress
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tissue-tissue interactions between myogenic precursors of craniofacial muscles and cranial neural crest cells (CNCCs). Here, we conducted gene expression profiling of the mandibular arch from mice at embryonic day E11.5 with a CNCC-specific conditional inactivation of the TGF-beta receptor type 1 gene Alk5. These mice provide a model of microglossia as well as disrupted extraocular and masticatory muscle development, which are congenital birth defects commonly observed in several syndromic conditions. To investigate the adverse effects of dysfunctional TGF-beta signaling on tissue-tissue interactions between CNCCs and myogenic precursors of craniofacial muscles, we analyzed mandibular arch tissue of mice with a CNCC-specific conditional inactivation of Alk5 (Wnt1-Cre; Alk5 fl/fl). We performed microarray analyses of the mandibular arch of Alk5 fl/fl control mice and Wnt1-Cre; Alk5 fl/fl mutant mice, collected at embryonic day E11.5 (n=4 per group).
2014-06-18 | E-GEOD-52357 | biostudies-arrayexpress
Project description:Purpose:The role of GDF11 in aging and cardiovascular diseases is controversial, and its function in cardiomyocytes(CMs) has not been fully explored. Methods: Total RNA was extracted from CMs using TRIzol® after CMs were transfected with shRNA-GDF11 and sh-Vector for 48h. Preparation of library and sequencing of transcriptome were carried out using Illu-mina HiSeq X Ten (Novogene Bioinformatics Technology Co., Ltd., Beijing, China). Results: Angiogenesis-related genes were the most downregulated when GDF11 was knockdown in mouse CMs. RNA-seq analysis showed that 3293 genes were downregulated and 3214 genes were upregulated when GDF11 was knockdown with shRNA-GDF11.
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Project description:The objective of this study was to identify transcriptional changes differentially regulated by GDF11 stimulation compared to TGFB1 Microarrays were used to capture the differential transcriptional response to acute GDF11 stimulation compared to acute TGFB1 stimulation
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