Ethanol effect on myoblast differentiation
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Michelle Arya
PROVIDER: E-GEOD-46492 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Expression profiling of C2C12 myoblast cells treated with ethanol during differentiation. Ethanol inhibits C2C12 differentiation. Results provide insight into signaling pathways altered by ethanol during differentiation.
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Project description:C2C12 mouse myoblasts (American Type Culture Collection, Manassas, VA) were maintained in growth medium (DMEM supplemented with 10% Fetal Bovine serum, Invitrogen Corporation, Carlsbad, CA) in 5% CO2. Cells were plated at a density of 40-50% in 100mm dishes. When cells reached ~90% confluency 24 hours later, they were switched to differentiation media (DMEM containing 2% horse serum; GIBCO, Invitrogen Corporation, Carlsbad, CA) which was subsequently changed every 48 hours. All cells were allowed to differentiate for 4 days with feeding every two days (day 0, 2, and 4). Beginning at day 4, control cells were re-fed every 48 hours whereas experimental cells were not re-fed. After an additional 4 days (8 days post differentiation), cells were harvested and total RNA was isolated from control and starved (non re-fed cells)
2007-10-23 | E-GEOD-1776 | biostudies-arrayexpress
Project description:C2C12 mouse myoblasts (American Type Culture Collection, Manassas, VA) were maintained in growth medium (DMEM supplemented with 10% Fetal Bovine serum, Invitrogen Corporation, Carlsbad, CA) in 5% CO2. Cells were plated at a density of 40-50% in 100mm dishes. When cells reached ~90% confluency 24 hours later, they were switched to differentiation media (DMEM containing 2% horse serum; GIBCO, Invitrogen Corporation, Carlsbad, CA) which was subsequently changed every 48 hours. All cells were allowed to differentiate for 4 days with feeding every two days (day 0, 2, and 4). Beginning at day 4, control cells were re-fed every 48 hours whereas experimental cells were not re-fed. After an additional 4 days (8 days post differentiation), cells were harvested and total RNA was isolated from control and "starved" (non re-fed cells) Keywords: repeat sample
2004-09-20 | GSE1776 | GEO
Project description:First, we aimed to identify genes whose transcript levels change at the onset of myogenic versus adipogenic differentiation of muscle precursors. We therefore compared RNA-seq results obtained from C2C12 cells differentiated for 1 day in myogenic and adipogenic medium. Out of these genes, we wanted to determine those whose expression was affected by altered Lsd1 levels. To this end, we performed RNA-seq in C2C12 cells upon LSD1 overexpression and Lsd1 knock-down in adipogenic medium and compared them to corresponding control cells.
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Project description:Mole (MSR) and fractional (FSR) synthesis rates of proteins during C2C12 myoblast differentiation were investigated. Myoblast cultures supplemented with D2O during 0-24 h or 72-96 h of differentiation were analysed by LC-MS/MS to calculate protein FSR and MSR after samples were spiked with yeast alcohol dehydrogenase (ADH1).
2020-10-22 | PXD021125 | Pride
Project description:In urodele amphibians, limb regeneration involves the dedifferentiation of muscle myotubes into single cells that may acquire pluripotent potential. We have employed small molecules (myoseverin and BIO) to attempt to reproduce this behavior in mammalian muscle culture. C2C12 myotubes derived from the C2C12 myoblast cell line were induced to undergo cellularization by myoseverin treatment, which destabilizes tubulin filaments. The GSK-3 inhibitor, BIO, was then used to induce dedifferentiation. Induce neuron formation; the cells were incubated with 250 nM reversine for 48 h, and neural induction media (DMEM/F12 supplemented with N2 (Invitrogen)) and 1.5 uM all-trans retinoic acid for 7 days. C2C12 murine myoblast cell line and 48 h 10 uM BIO treated C2C12 cellulate (derived by 20 M myoseverin treatment for 48 h) C2C12 myoblasts were differentiated into myotubes with 2%horse serum in DMEM for 8 days (from 2-4 d, 10 uM AraC treatment was also used to kill any remaining myoblasts). Next, myotubes were cellularized by 20 uM myoseverin treatment for 48 h. 24 h after myoseverin treatment, myotubes were treated with 10 uM BIO for 2d.
2011-12-08 | E-GEOD-34238 | biostudies-arrayexpress
Project description:Wnt/β-catenin signaling is involved in various aspects of skeletal muscle development and regeneration. In addition, Wnt3a and β-catenin are required for muscle-specific gene transcription in embryonic carcinoma cells and satellite-cell proliferation during adult skeletal muscle regeneration. Downstream targets of canonical Wnt signaling are cyclin D1 and c-myc. However, both target genes are suppressed during differentiation of mouse myoblast cells, C2C12. Underlying molecular mechanisms of β-catenin signaling during myogenic differentiation remain unknown. Using C2C12 cells, we examined intracellular signaling and gene transcription during myoblast proliferation and differentiation. We confirmed that several Wnt signaling components, including Wnt9a, Sfrp2 and porcupine, were consistently upregulated in differentiating C2C12 cells. Troponin T-positive myotubes were decreased by Wnt3a overexpression, but not Wnt4. TOP/FOP reporter assays revealed that co-expression with Wnt4 reduced Wnt3a-induced luciferase activity, suggesting that Wnt4 signaling counteracted Wnt3a signaling in myoblasts. FH535, a small-molecule inhibitor of β-catenin/Tcf complex formation, reduced basal β-catenin in cytoplasm and decreased myoblast proliferation. K252a, a protein kinase inhibitor, increased membrane-bound β-catenin and enhanced myoblast fusion. Treatments with K252a or Wnt4 resulted in increased cytoplasmic vesicles containing phosphorylated β-catenin (Tyr654) during myogenic differentiation. These results suggest that various Wnt ligands control subcellular β-catenin localization, which regulate myoblast proliferation and myotube formation. Wnt signaling via β-catenin likely acts as a molecular switch that regulates the transition from cell proliferation to myogenic differentiation.
2011-07-15 | GSE30077 | GEO
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. Experiment Overall Design: Cell culture - Mouse C2C12 myoblasts (ATCC, Manassas, VA) were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with 20% fetal bovine serum (Invitrogen), at a confluency of 60-70%. To initiate differentiation, cells were allowed to reach 100% confluency and medium was changed to DMEM containing 2% horse serum (Invitrogen) and changed every 2 days. Full differentiation, with myotube fusion and spontaneous twitching, was observed at 5 days. Fatty acid stock preparation - Fatty acids were dissolved in 0.1 N sodium hydroxide (final concentration 100 mM) at 65 degrees C for 2 hours and then complexed with 10% fatty acid-free BSA, yielding a final stock of 5 mM. Three replicates for each fatty-acid. Microarray analysis - RNA was isolated as described from C2C12 myotubes treated overnight with 500 uM palmitate or 1% BSA, and cRNA was synthesized. 10 mg of cRNA were hybridized to Affymetrix mouse 430A 2.0 arrays. Intensity values were quantified using MAS 5.0 software. MAPPFinder (www.genmapp.org) was used to integrate expression data with known pathways. Transcription profiling of mouse C2C12 myotubes treated overnight with 500 uM palmitate or 1% BSA to identify mediators of obesity-linked reductions in PGC-1.
2007-11-15 | E-GEOD-6766 | biostudies-arrayexpress
Project description:Wnt/M-NM-2-catenin signaling is involved in various aspects of skeletal muscle development and regeneration. In addition, Wnt3a and M-NM-2-catenin are required for muscle-specific gene transcription in embryonic carcinoma cells and satellite-cell proliferation during adult skeletal muscle regeneration. Downstream targets of canonical Wnt signaling are cyclin D1 and c-myc. However, both target genes are suppressed during differentiation of mouse myoblast cells, C2C12. Underlying molecular mechanisms of M-NM-2-catenin signaling during myogenic differentiation remain unknown. Using C2C12 cells, we examined intracellular signaling and gene transcription during myoblast proliferation and differentiation. We confirmed that several Wnt signaling components, including Wnt9a, Sfrp2 and porcupine, were consistently upregulated in differentiating C2C12 cells. Troponin T-positive myotubes were decreased by Wnt3a overexpression, but not Wnt4. TOP/FOP reporter assays revealed that co-expression with Wnt4 reduced Wnt3a-induced luciferase activity, suggesting that Wnt4 signaling counteracted Wnt3a signaling in myoblasts. FH535, a small-molecule inhibitor of M-NM-2-catenin/Tcf complex formation, reduced basal M-NM-2-catenin in cytoplasm and decreased myoblast proliferation. K252a, a protein kinase inhibitor, increased membrane-bound M-NM-2-catenin and enhanced myoblast fusion. Treatments with K252a or Wnt4 resulted in increased cytoplasmic vesicles containing phosphorylated M-NM-2-catenin (Tyr654) during myogenic differentiation. These results suggest that various Wnt ligands control subcellular M-NM-2-catenin localization, which regulate myoblast proliferation and myotube formation. Wnt signaling via M-NM-2-catenin likely acts as a molecular switch that regulates the transition from cell proliferation to myogenic differentiation. Control cells (day 0) prior to differentiation induction with n=4; differentiated for two days with n=3; differentiated for four days with n=3.
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Project description:The effects of ethanol may vary from induction of apoptosis to the inhibition of proliferation, differentiation, migration or other function. The complex and diverse response of fetal cells to ethanol has prompted us to use a bioinformatics approach to study the effect of ethanol on fetal stem cells derived from the amniotic fluid-derived (AFSC). To characterize the global response of human AFSC to ethanol, gene expression profiles of AFSC treated with or without 100mM ethanol for 48 hours were analyzed. Keywords: stem cells, amniotic fluid-derived stem cells, ethanol, alcohol
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