Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Palmitate-induced inhibition of C2C12 insulin pathway modifies the release of exosomes and their biological actions on muscle cells

ABSTRACT: Exosomes are cell-released bioactive nanovesicles now considered as new partners in the inter-organ cross-talks. The possibility that skeletal muscle (SkM)-derived exosomes act as a mode of systemic communication has hitherto never been described. Thus, in this study we have tested the hypothesis that through the exosomal route, muscle cells might transmit specific signals during insulin-resistance.

ORGANISM(S): Mus musculus

PROVIDER: GSE52048 | GEO | 2016/11/03

SECONDARY ACCESSION(S): PRJNA226583

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Muscle-released exosomes modulate gene expressions in beta-cells in mice

Project description:Exosomes are cell-released bioactive nanovesicles now considered as new partners in the inter-organ cross-talks. The possibility that skeletal muscle (SkM)-derived exosomes act as a mode of systemic communication has been described. Thus, in this study we have tested the hypothesis that through the exosomal route, muscle might transmit specific signals during insulin-resistance.

2017-07-14 | GSE59429 | GEO

Nrf2 bindng in C2C12 myotubes

Project description:Nrf2 (NF-E2-related-factor-2) contributes to the maintenance of glucose homeostasis in vivo. Nrf2 suppresses blood glucose levels by protecting pancreatic Î²-cells from oxidative stress and improving peripheral tissue glucose utilization. To elucidate the molecular mechanisms by which Nrf2 contributes to the maintenance of glucose homeostasis, we generated skeletal muscle (SkM)-specific Keap1-knockout (Keap1MuKO) mice that express abundant Nrf2 in SkM and then examined Nrf2-target gene expression in this tissue. In Keap1MuKO mice, blood glucose levels were significantly downregulated, and the levels of glycogen branching enzyme (Gbe1) mRNA, along with those of glycogen branching enzyme (GBE) protein, were significantly upregulated in mouse SkM. Consistent with this result, chemical Nrf2-inducers promoted Gbe1 mRNA expression in both mouse SkM and C2C12 myotubes. Chromatin-immunoprecipitation analysis demonstrated that Nrf2 binds the Gbe1 upstream promoter regions. In Keap1MuKO mice, muscle glycogen content was strongly reduced, and forced GBE expression in C2C12 myotubes promoted glucose uptake. Therefore, our results demonstrate that Nrf2-induction in SkM increases GBE expression and reduces muscle glycogen content, resulting in improved glucose tolerance. Chromatin occupancy of Nrf2 under CDDO-Im-treated condition were generated by deep sequencing, in dupliplicate

2016-04-06 | E-GEOD-78780 | biostudies-arrayexpress

Nrf2 bindng in C2C12 myotubes

Project description:Nrf2 (NF-E2-related-factor-2) contributes to the maintenance of glucose homeostasis in vivo. Nrf2 suppresses blood glucose levels by protecting pancreatic β-cells from oxidative stress and improving peripheral tissue glucose utilization. To elucidate the molecular mechanisms by which Nrf2 contributes to the maintenance of glucose homeostasis, we generated skeletal muscle (SkM)-specific Keap1-knockout (Keap1MuKO) mice that express abundant Nrf2 in SkM and then examined Nrf2-target gene expression in this tissue. In Keap1MuKO mice, blood glucose levels were significantly downregulated, and the levels of glycogen branching enzyme (Gbe1) mRNA, along with those of glycogen branching enzyme (GBE) protein, were significantly upregulated in mouse SkM. Consistent with this result, chemical Nrf2-inducers promoted Gbe1 mRNA expression in both mouse SkM and C2C12 myotubes. Chromatin-immunoprecipitation analysis demonstrated that Nrf2 binds the Gbe1 upstream promoter regions. In Keap1MuKO mice, muscle glycogen content was strongly reduced, and forced GBE expression in C2C12 myotubes promoted glucose uptake. Therefore, our results demonstrate that Nrf2-induction in SkM increases GBE expression and reduces muscle glycogen content, resulting in improved glucose tolerance.

2016-04-06 | GSE78780 | GEO

Differentially expressed genes of C2C12 cells influenced by murine pancreatic cancer derived exosomes

Project description:Mice pancreatic cancer derived exosomes(KPC-exosomes) could induce skeletal muscle cells(C2C12) insulin resistance and exosomal microRNAs (miRNAs) may exert an important effect (Sci Rep. 2017;7(1):5384). The data set GSE95741 provided the differentially expressed micro RNAs. In this work, we aim to detect the differentially expressed genes and explore the intrinsic link.

2022-01-01 | GSE174058 | GEO

C2C12 Myotubes in response to Palmitate

Project description:To identify mediators of obesity-linked reductions in PGC-1, we tested the effects of cellular nutrients in C2C12 myotubes. While overnight exposure to high insulin, glucose, glucosamine, or amino acids had no effect, saturated fatty acids (FA) potently reduced PGC-1a and b mRNA expression. Keywords: Nutrient Effect

2007-01-18 | GSE6766 | GEO

Integrative Analysis of ovarian cancer cell behavior reveals a miRNA signature associated with Intrinsic Platinum Resistance in ovarian cancer.

Project description:The aim of this study was to identify a set of miRNAs which are associated with chemotherapy resistance in ovarian cancer, and to evaluate if these miRNAs are enrich in small nanovesicles, called exosomes, released from ovarian cancer cells.

2021-05-25 | GSE114920 | GEO

Global tibialis anterior skeletal muscle transcript data from male Carm1 skm-/- (HSAcre Tg/0 x Floxed Carm1) and Carm1 skm+/+ mice (HSAcre 0/0 x Floxed Carm1) on a chow diet.

Project description:Transcript data from tibialis anterior muscle from male muscle-specific Coactivator-Associated Arginine Methyltransferase 1 (Carm1 ) knockout mice (Carm1 skm-/- ) and wild-type mice (Carm1 skm+/+) generated by using the Cre-loxP system (on a C57BL6J/129 background) with HSA-Cre mice (from Jackson laboratories). We used RNA-Seq to detail the effects of muscle-specific loss of Carm1 on the global program of gene expression in tibialis anterior muscle.

2022-08-24 | GSE189351 | GEO

In vitro contraction protects against palmitate-induced insulin resistance in C2C12 myotubes.

Project description: Not available

| S-EPMC5792169 | biostudies-literature

Multimodality Assessment of HFpEF Skeletal Muscle Reveals Differences in the Machinery of Energy Fuel Metabolism

Project description:Aims: Skeletal muscle (SkM) abnormalities may impact exercise capacity in patients with Heart Failure with Preserved Ejection Fraction (HFpEF). We sought to quantify differences in SkM oxidative phosphorylation capacity (OxPhos), fiber composition, and the SkM proteome between HFpEF, hypertensive (HTN), and Healthy participants. Methods: 59 subjects (20 Healthy, 19 HTN, 20 HFpEF) performed a maximal-effort cardiopulmonary exercise test to define peak oxygen consumption (VO2, peak), ventilatory threshold (VT), and VO2 efficiency (ratio of total work performed to O2 consumed). SkM OxPhos was assessed using Creatine Chemical-Exchange Saturation Transfer (CrCEST, n=51), which quantifies unphosphorylated Cr, before and after plantar flexion exercise. The half-time of Cr recovery (t1/2, Cr) was taken as a metric of in vivo SkM OxPhos. In a subset of subjects (Healthy=13, HTN=9, HFpEF=12), percutaneous biopsy of the vastus lateralis was performed for myofiber typing, mitochondrial morphology, and proteomic and phosphoproteomic analysis. Results: HFpEF subjects demonstrated lower VO2,peak, VT, and VO2 efficiency than either control group (all p<0.05). The t1/2, Cr was significantly longer in HFpEF (p=0.005), indicative of impaired SkM OxPhos, and correlated with cycle ergometry exercise parameters. HFpEF SkM contained fewer Type-I myofibers (p=0.003). Proteomic analyses demonstrated (a) reduced levels of proteins related to OxPhos that correlated with exercise capacity and (b) reduced ERK signaling in HFpEF. Conclusions: HFpEF patients demonstrate impaired functional capacity and SkM OxPhos. Reductions in the proportions of type 1 myofibers, proteins required for OxPhos, and altered phosphorylation signaling in the SkM may contribute to exercise intolerance in HFpEF.

2021-03-30 | PXD025092 | Pride

miRNA profiling of Pax3-FOXO1-C2C12-derived exosomes compared to control C2C12 cells, using the Affymetrix GeneChip miRNA 3.0 array

Project description:C2C12 mouse myoblasts were transduced with either PAX3-FOXO1 expression vector (P3F-C2C12), a system that is commonly used to study the more aggressive alveolar rhabdomyosarcoma subtype, or empty vector (Ctrl-C2C12). Exosomes were isolated from both cell lines by differential centrifugation, and exosomal markers were characterized by western blot. Then, the Affymetrix GeneChip miRNA 3.0 array was used to identify the miRNA content of the extracted exosomes where the differentially deregulated miRNA (either enriched or depleted) in P3F-C2C12 exosomes were determined relative to Ctrl-C2C12 exosomes. Results showed that PAX3-FOXO1 fusion gene alters the content of exosomes and that the enriched miR-486-5p is a downstream effector of PAX3-FOXO1 in mediating the oncogenic effects of exosome-mediated paracrine signaling in this setting.

2019-12-01 | E-MTAB-7646 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data