Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA267828 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To confirm changing C2C12 cells genetic profile and losing their myogenic ability, we investigated the combined effect of EPA and DHA on the relative expression of genes regulating the terminal differentiation of myoblast into mature multinucleated myotubes.
2020-06-24 | PXD016929 | Pride
Project description:Gene Expression Profiling of C2C12 Myoblast Differentiation
| PRJNA123703 | ENA
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.
2011-07-15 | E-GEOD-30077 | 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:We newly identified skeletal muscle differentiation-associated miRNAs by comparing miRNA expression profile between C2C12 cell and Wnt4-overexpressing C2C12 cell. miR-487b, miR-3963 and miR-6412 are significantly down-regulated in differentiating C2C12 cells, and transfection of their mimics resulted in reduced expression of myogenic differentiation markers including Troponin T, myosin heavy chain fast and slow type. Single analysis for each condition (proliferating C2C12 cells, differentiating C2C12 cells, proliferating Wnt4-overexpressing C2C12 subline cells
2015-11-24 | E-GEOD-63454 | biostudies-arrayexpress
Project description:Controlled myogenic differentiation is integral to the development, maintenance and repair of skeletal muscle, necessitating precise regulation of myogenic progenitors and resident stem cells. The transformation of proliferative muscle progenitors into multinuclear syncytia involves intricate cellular processes driven by cytoskeletal reorganization. While actin and microtubles have been extensively studied, we illuminate the role of septins, an essential yet still often overlooked cytoskeletal component, in myoblast architecture. Notably, Septin9 emerges as a critical regulator of myoblast differentiation during the initial commitment phase. Knock-down of Septin9 in C2C12 cells and primary mouse myoblasts accelerates the transition from proliferation to committed progenitor transcriptional programs. Furthermore, we unveil significant reorganization and downregulation of Septin9 during myogenic differentiation. Collectively, we propose that filmamentous septin structures and their orchestrated reorganization in myoblasts are part of a temporal regulatory mechanism governing the differentiation of myogenic progenitors. This study sheds light on the dynamic interplay between cytoskeletal components underlying controlled myogenic differentiation.
2024-07-17 | GSE272316 | GEO
Project description:Interaction of Wnt signaling with Smad signaling during myogenic differentiation in mouse myoblast cells
| PRJNA174081 | ENA
Project description:We newly identified skeletal muscle differentiation-associated miRNAs by comparing miRNA expression profile between C2C12 cell and Wnt4-overexpressing C2C12 cell. miR-487b, miR-3963 and miR-6412 are significantly down-regulated in differentiating C2C12 cells, and transfection of their mimics resulted in reduced expression of myogenic differentiation markers including Troponin T, myosin heavy chain fast and slow type.
2015-11-24 | GSE63454 | GEO
Project description:To study the gene expression profile difference caused by miR-322/-503 overexpression in the myoblast differentiation of DM1 group, we performed RNA-seq on the total RNA samples collected from the in vitro myoblast differentiation day 4 of control and miR-322/-503 overexpressing DM1 C2C12 cell models. The DM1 cell model was bulit by stably transfecting C2C12 cells with GFP-CUG200 plasmid. Each group contained three biological replicates. The expression matrix was obtained by Hisat2 followed by Stringtie.
2022-03-21 | GSE189897 | GEO