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Dataset results
291 results for “myoblasts”
Data for a publication "LIPSS pattern induced by polymer surface instability for myoblast cell guidance"
<p>The data set for contains data used in the article "LIPSS pattern induced by polymer surface instability for myoblast cell guidance".</p> <p><strong>Versions:</strong></p> <p><em><strong>V2: </strong>The current version contains reorganized file folders and is supplemented by the data found in the publication "LIPSS pattern induced by polymer surface instability for myoblast cell guidance". The dataset newly contains contact angle, cytocompatibility tests, FTIR analyses or Zeta potential results.</em></p> <p><strong>Article abstract</strong></p> <p>The presented study highlights the efficiency of employing a KrF excimer laser to create diverse types of periodic nanostructures (LIPSS – laser induced periodic surface structures) on polyether ether ketone (PEEK) and polyethylene naphthalate (PEN) substrates. LIPSS structures are very important both in tissue engineering and find also strong application in the field of sensor construction, and SERS analysis. By exposing the polymer films below their ablation threshold to laser fluence ranging from 4 to 16 mJ·cm<sup>-2</sup> at 6,000 pulses, we studied both single-phase exposure at beam incidence angles of 0° and 45°, and two-phase exposure. Atomic force microscopy analysis revealed that the laser-treated samples contained distinctive periodic patterns such as waves, globules, and pod-like structures each exhibiting unique surface roughness. Moreover, using analytical methods like EDS and XPS shed light on the changes in the atomic composition, specifically focusing on the C and O elements, as a result of laser exposure. Notably, in almost all cases, we observed an increase in oxygen percentage on the sample surfaces. This increase not only led to a decrease in the contact angle with water but also lowered the zeta potential value, thus showing that the modified samples have enhanced hydrophilicity of the surface and altered electrostatic properties. Last but not least, the samples were assessed for biocompatibility; we studied the interaction of the prepared replicates with mouse myoblasts (C2C12). The impact of globular/dot structures on the cell growth in comparison to pristine or linear LIPSS-patterned surfaces was determined. The linear pattern (LIPSS) induced the myoblast cell alignment along the pattern direction, while dot/globular pattern even enhanced the cytocompatibility compared to LIPSS samples. Through this comprehensive analysis, the research underscores the multifaceted implications of employing KrF excimer laser-induced nanostructures, ranging from surface morphology alterations to biocompatibility enhancements, thus, opening new avenues for advanced material engineering.</p>
Optimising C2C12 muscle myoblast transfection with polyethylenimine (PEI) or Lipofectamine-2000
<p>Optimisation of DNA transfection of the C2C12 muscle myoblast cell line, comparing use of polyethylenimine (PEI) and Lipofectamine-2000 with varying treatment conditions. </p>
Gene Enhancer Predictions in C2C12 (Mouse Myoblast)
<p>This file contains the complete enhancer prediction output of the analysis done in this study published on Nature Communications:</p> <p><a href="https://www.nature.com/articles/s41467-025-57758-x" target="_blank" rel="noopener">https://www.nature.com/articles/s41467-025-57758-x</a></p> <p>using the Activity by Contact Model following the pipeline described here: <a href="https://github.com/broadinstitute/ABC-Enhancer-Gene-Prediction">https://github.com/broadinstitute/ABC-Enhancer-Gene-Prediction</a></p> <p>To be used in this analysis, a genomewide Hi-C interaction matrix was generated with <a>Juicer </a> v1.6, expression counts for each gene were generated with STAR v2.7.10b and <a>Rsubread</a> v2.8.2, and the sequence alignment maps of ATAC-seq and H3K27ac ChIP-seq were generated with NextGenMap v0.5.5, all using raw sequencing reads downloaded from <a>SRA</a>: Hi-C (SRR16220088), RNA-seq (SRR074113 and SRR074114), <a>ATAC-seq (SRR2999996) and H3K27ac ChIP-seq (SRR358589, SRR358590, and SRR358591).</a></p> <p><a>The chromosome coordinates are of the GRCm38 - mm10 assembly, and the gene IDs are from ENSEMBL annotation.</a></p> <p>Please use the Version 3, and for more information please refer to our publication that used these enhancer predictions.</p>
DUX4 expression activates JNK and p38 MAP kinases in myoblasts: MAJIQ splicing results
<p>Facioscapulohumoral muscular dystrophy (FSHD) is caused by misexpression of the DUX4 transcription factor in skeletal muscle that results in transcriptional alterations, abnormal phenotypes, and cell death. To gain insight into the kinetics of DUX4-induced stresses, we activated DUX4 expression in myoblasts and performed longitudinal RNA sequencing (GEO GSE205421) paired with proteomics and phosphoproteomics (MassIVE MSV000089812). This analysis revealed changes in cellular physiology including DNA damage and altered mRNA splicing. Phosphoproteomic analysis uncovered widespread changes in protein phosphorylation rapidly following DUX4 induction indicating that alterations in kinase signaling may play a role in DUX4-mediated stress and cell death. Indeed, we demonstrate that two stress-responsive MAP kinase pathways, JNK and p38, are activated in response to DUX4 expression. Inhibition of each of these pathways ameliorated DUX4-mediated cell death in myoblasts. These findings uncover JNK as a novel pathway involved in DUX4-mediated cell death as well as provide additional insights into the role of the p38 pathway, a clinical target for the treatment of FSHD.</p>
Gene Enhancer Predictions in C2C12 (Mouse Myoblast)
<p>This file contains the complete enhancer prediction output of the analysis done in this study published on Nature Communications:</p> <p><a href="https://www.nature.com/articles/s41467-025-57758-x" target="_blank" rel="noopener">https://www.nature.com/articles/s41467-025-57758-x</a></p> <p>using the Activity by Contact Model following the pipeline described here: <a href="https://github.com/broadinstitute/ABC-Enhancer-Gene-Prediction">https://github.com/broadinstitute/ABC-Enhancer-Gene-Prediction</a></p> <p>To be used in this analysis, a genomewide Hi-C interaction matrix was generated with <a>Juicer </a> v1.6, expression counts for each gene were generated with STAR v2.7.10b and <a>Rsubread</a> v2.8.2, and the sequence alignment maps of ATAC-seq and H3K27ac ChIP-seq were generated with NextGenMap v0.5.5, all using raw sequencing reads downloaded from <a>SRA</a>: Hi-C (SRR16220088), RNA-seq (SRR074113 and SRR074114), <a>ATAC-seq (SRR2999996) and H3K27ac ChIP-seq (SRR358589, SRR358590, and SRR358591).</a></p> <p><a>The chromosome coordinates are of the GRCm38 - mm10 assembly, and the gene IDs are from ENSEMBL annotation.</a></p> <p> </p> <p>This research was funded in whole or in part by the Austrian Science Fund (FWF) [P29713-B28, P32512-B and P36503-B] to Roland Foisner and a doctorate program funded by the Austrian Science Fund (FWF) [W1261-B28].</p> <p> </p> <p>For more information please refer to our publication that used these enhancer predictions titled:</p> <p>MyoD1 localization at the nuclear periphery is mediated by association of WFS1 with active enhancers</p>
Autologous Myoblast Intrasphincteric Injection for Fecal Incontinence
ClinicalTrials.gov study NCT01523522. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Safety and Efficacy Study of Intrasphincteric Autologous Myoblast Injection to Treat Stress Urinary Incontinence
ClinicalTrials.gov study NCT01355133. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Treatment of Dysphagia in Oculopharyngeal Muscular Dystrophy by Autologous Transplantation of Myoblasts
ClinicalTrials.gov study NCT00773227. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Transplantation of Myoblasts to Duchenne Muscular Dystrophy (DMD) Patients
ClinicalTrials.gov study NCT02196467. IPD Sharing: YES. Countries: 1. Publications: 4.
DUX4 expression activates JNK and p38 MAP kinases in myoblasts: MAJIQ splicing results
Open the record for dataset details and reuse information.
Data for publication: "Plasma-Activated Polydimethylsiloxane Microstructured Pattern with Collagen for Improved Myoblast Cell Guidance"
<p>Abstract</p> <p>We focused on polydimethylsiloxane (PDMS) as a substrate for replication, micropatterning, and construction of biologically active surfaces. The novelty of this study is based on the combination of the argon plasma exposure of a micropatterned PDMS scaffold, where the plasma served as a strong tool for subsequent grafting of collagen coatings and their application as cell growth scaffolds, where the standard was significantly exceeded. As part of the scaffold design, templates with a patterned microstructure of different dimensions (50 × 50, 50 × 20, and 30 × 30 μm2) were created by photolithography followed by pattern replication on a PDMS polymer substrate. Subsequently, the prepared microstructured PDMS replicas were coated with a type I collagen layer. The sample preparation was followed by the characterization of material surface properties using various analytical techniques, including scanning electron microscopy (SEM), energy-dispersive X-ray spectroscopy (EDS), and X-ray photoelectron spectroscopy (XPS). To evaluate the biocompatibility of the produced samples, we conducted studies on the interactions between selected polymer replicas and micro- and nanostructures and mammalian cells. Specifically, we utilized mouse myoblasts (C2C12), and our results demonstrate that we achieved excellent cell alignment in conjunction with the development of a cytocompatible surface. Consequently, the outcomes of this research contribute to an enhanced comprehension of surface properties and interactions between structured polymers and mammalian cells. The use of periodic microstructures has the potential to advance the creation of novel materials and scaffolds in tissue engineering. These materials exhibit exceptional biocompatibility and possess the capacity to promote cell adhesion and growth.</p> <p> </p>
Data Analysis Scripts Bovine Myoblasts
<p>Data analysis scripts for the proteome and transcriptome analysis of bovine myoblasts.</p> <p>Raw & processed mass spectrometry data for proteome analysis can be accessed under PXD052959.</p>
Syndecan-4 proteoglycan modulates glucose uptake and insulin sensitivity in myoblasts
<p>Skeletal muscle glucose uptake is required for cellular metabolism and normalization of postprandial blood glucose levels. Transmembrane heparan sulfate proteoglycan syndecan-4 (SDC4) is important for muscle regeneration, cell interaction and structure, and it affects whole body metabolism, although the mechanism remains unclear. In this study, we demonstrated that SDC4 knock down increases glucose uptake by mammalian myoblasts (i.e., activated satellite cells). Silencing SDC4 increased the phosphorylation AS160 (Akt substrate of 160 kDa or TBC1D4), an important element of glucose transporter type 4 (GLUT4) translocation, and GLUT4 levels. These changes increased 2–deoxy-2–(<sup>18</sup>F)fluoro-D-glucose uptake by C2C12 myoblasts independent of insulin treatment. Mitochondrial routine respiration, electron transport system, reserve capacity, and oxidative phosphorylation were also increased following SDC4 silencing. SDC4 knockdown cells exhibited a higher GLUT4 density along the plasma membrane compared with behind it. Super-resolution direct stochastic optical reconstruction microscopy (dSTORM) imaging revealed an increased number of skeletons of the actin network following insulin treatment, but not in SDC4-silenced cells. Notably, knocking down SDC4 increased the insulin sensitivity of the cells. Our results suggest that this new mechanism can increase glucose uptake through insulin-independent signal transduction.</p> <p>Proteomics data.</p>
Transcriptional profiling of MLL5 Knock down vs. control C2C12 myoblasts (S phase enriched)
GEO Series GSE14931. Mus musculus. 2 samples. Type: Expression profiling by array.
Loss of Antp function in Drosophila flight muscle precursors : RNAi in larval wing disc-associated myoblasts
GEO Series GSE268578. Drosophila melanogaster. 4 samples. Type: Expression profiling by high throughput sequencing.
Genome-wide analysis of mRNA expression in control and ChRO1 depleted C2C12 (Myoblasts and Myotubes)
GEO Series GSE104304. Mus musculus. 4 samples. Type: Expression profiling by array.
Microtranscriptome changes upon Human Skeletal Myoblasts differentiation
GEO Series GSE147838. Homo sapiens. 6 samples. Type: Non-coding RNA profiling by high throughput sequencing.
Mitochondrial dysfunction and consequences in calpain-3-deficient muscle myoblasts
GEO Series GSE199620. Mus musculus. 6 samples. Type: Expression profiling by array.
Enhancing Skeletal Muscle Fiber Types Transition through Substrate Coating Alteration in Myoblast Cell Culture
GEO Series GSE279968. Mus musculus. 12 samples. Type: Expression profiling by high throughput sequencing.
Identification of binding sites of the Six1 transcription factor in mouse primary myoblasts and myotubes
GEO Series GSE175999. Mus musculus. 4 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.