Project description:PFOS has been shown to perturb metabolism in skeletal muscle according to previous research from our lab. To determine the transciptional changes associated with PFOS exposure, C2C12 skeletal myoblasts were exposed to PFOS for 24 hours. Changes in several metabolic pathways were seen, including amino acid and glucose metabolism.
Project description:The purpose of this project was to investigate the effects of PFOS on skeletal muscle in vivo. To perform this work, Cyp2b-null and hCYP2B6-Tg mice were treated with 0, 1, or 10 mg/kg/day PFOS for 21 days. Gastrocnemius muscle was collected during necropsy and various assays were performed. RNA seq was performed to determine what gene expression changes occured due to PFOS treatment and the difference between genotypes.
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: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: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: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:LMNA mutation R482L cause classical familial partial lipodystrophy of Dunnigan type (FPLD2). FPLD is a severe metabolic disorder that often leads to cardiovascular and skeletal muscle complications. How LMNA mutations affect functional properties of skeletal muscles is still not understood. In the present project we investigated the LMNA-R482L mutation-specific alterations in mouse C2C12 line of myoblasts using single cell RNA sequencing (scRNA-seq). We showed the heterogeneity of C2C12 myoblasts cell line prior the differentiation, and compositional and transcriptional changes in LMNA-R482L C2C12 myoblasts comparing to LMNA-WT.
Project description:To determine the lncRNA expression profile in C2C12 myoblasts and myotubes, we used mouse lncRNA microarray from Arraystar to examine the expression of lncRNAs in C2C12 myoblasts and myotubes.
Project description:To determine the circRNA expression profile in C2C12 myoblasts and myotubes, we used mouse circRNA microarray from Arraystar to examine the expression of circRNAs in C2C12 myoblasts and myotubes.