Effect of LSD1 inhibition on differentiating C2C12 myoblasts
Ontology highlight
ABSTRACT: Analysis of differentiating C2C12 myoblasts treated with two LSD1 specific inhibitors. We found LSD1 is an important regulator of oxidative phenotypes in skeletal muscle cells. Results provide insight into the molecular mechanisms underlying roles of LSD1 in myocytes.
Project description:Analysis of differentiating LSD1-KD C2C12 myoblasts. We found LSD1 is an important regulator of oxidative phenotypes in skeletal muscle cells. Results provide insight into the molecular mechanisms underlying roles of LSD1 in myocytes.
Project description:ChIP-seq analysis of LSD1 in C2C12 cells. We found that LSD1 directly regulates the expression of fiber and metabolism genes during myogenesis. Results provide insight into the molecular mechanisms of myogenesis.
Project description:ChIP-seq analysis of LSD1 in C2C12 cells. We found that LSD1 directly regulates the expression of fiber and metabolism genes during myogenesis. Results provide insight into the metabolic prgramming mechanisms of myogenesis.
Project description:C2C12 myoblast is a model that has been used extensively to study the process of skeletal muscle differentiation. Proteomics has advanced our understanding of skeletal muscle biology and the process of myogenesis. However, there is still no deep coverage of C2C12 myoblast proteome, which is important for the understanding of key drivers for the differentiation of skeletal muscle cells. Here, we conducted a multi-dimensional proteome profiling with TiSH strategy to get a comprehensive analysis of proteome, phosphoproteome and N-linked sialylated glycoproteome of C2C12 myoblasts. A total of 8313 protein groups were identified in C2C12 myoblasts, including 7827 protein groups from non-modified peptides, 3803 phosphoproteins and 977 formerly N-linked sialylated glycoproteins.
Project description:ChIP-seq analysis of methylated H3K4 in LSD1-inhibited C2C12 cells. We found that LSD1 widely regulates the methylation levels of H3K4. Results provide insight into the molecular mechanisms of regulation of histone modification in myogenesis.
Project description:Proteosome inhibitors such as bortezomib (BTZ) have been used to treat muscle wasting in animal models. However, direct effect of BTZ on skeletal muscle cells has not been reported. In the present study, our data showed that C2C12 cells exhibited a dose-dependent decrease in cell viability in response to increasing concentrations of BTZ. We used microarrays to detail the differentially expressed genes in c2c12 myoblasts with different culture conditions.
Project description:GDF8 (myostatin) is a unique cytokine strongly affecting the skeletal muscle phenotype in human and animals. The aim of the present study was to elucidate the molecular mechanism of myostatin influence on the differentiation of mouse C2C12 myoblasts, using the global-transcriptome analysis with the DNA microarray technique. Treatment with exogenous GDF8 strongly affected the growth and development of C2C12 mouse myoblasts. This was manifested by the inhibition of proliferation and differentiation as well as the impairment of cell fusion. DNA microarray analysis revealed 778 genes regulated by GDF8 in differentiating myoblasts. Ontological analysis revealed their involvement in 17 types of biological processes, 10 types of molecular functions and 68 different signaling pathways. The effect of GDF8 was mainly mediated by the disruption of the cell cycle, calcium and insulin signaling pathways and expression of cytoskeletal and muscle specific proteins.