Effect of myocardin mis-expression in human skeletal myoblasts
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE3378 | GEO | 2005/10/27
SECONDARY ACCESSION(S): PRJNA93507
REPOSITORIES: GEO
Similar Datasets
Project description:transcriptional effects of mis-expression of full length (935) myocardin in growing human skeletal myoblasts Experiment Overall Design: Compare transcriptional profiles of Ad-myocardin infected SKM5 cells with that of Ad-B-gal infected cells
2008-06-12 | E-GEOD-3378 | biostudies-arrayexpress
Project description:Myocardin-related transcription factors (MRTFs) play a central role in the regulation of actin expression and cytoskeletal dynamics. Stimuli that promote actin polymerization allow for shuttling of MRTFs to the nucleus where they activate serum response factor (SRF), a regulator of actin and other cytoskeletal protein genes. SRF is an essential regulator of skeletal muscle differentiation and numerous components of the muscle sarcomere, but the potential involvement of MRTFs in skeletal muscle development has not been examined. We explored the role of MRTFs in muscle development in vivo by generating mutant mice harboring a skeletal muscle-specific deletion of MRTF-B and a global deletion of MRTF-A. These double knockout (dKO) mice were able to form sarcomeres during embryogenesis. However, the sarcomeres were abnormally small and disorganized, causing skeletal muscle hypoplasia and perinatal lethality. Transcriptome analysis demonstrated dramatic dysregulation of actin genes in MRTF dKO mice, highlighting the importance of MRTFs in actin cycling and myofibrillogenesis. MRTFs were also necessary for the survival of skeletal myoblasts and for the efficient formation of intact myotubes. Our findings reveal a central role for MRTFs in sarcomere formation during skeletal muscle development and point to the potential involvement of these transcriptional coactivators in skeletal myopathies. Gene expression profile was generated comparing wild type (WT) and HSA-Cre, MRTF-A/B double knockout mice, by deep seqencing, with three biological replicates, using Illumina HiSeq 2500.
2016-08-02 | E-GEOD-84063 | biostudies-arrayexpress
Project description:Effect of myocardin mis-expression in human skeletal myoblasts
| PRJNA93507 | ENA
Project description:Myocardin-related transcription factors (MRTFs) play a central role in the regulation of actin expression and cytoskeletal dynamics. Stimuli that promote actin polymerization allow for shuttling of MRTFs to the nucleus where they activate serum response factor (SRF), a regulator of actin and other cytoskeletal protein genes. SRF is an essential regulator of skeletal muscle differentiation and numerous components of the muscle sarcomere, but the potential involvement of MRTFs in skeletal muscle development has not been examined. We explored the role of MRTFs in muscle development in vivo by generating mutant mice harboring a skeletal muscle-specific deletion of MRTF-B and a global deletion of MRTF-A. These double knockout (dKO) mice were able to form sarcomeres during embryogenesis. However, the sarcomeres were abnormally small and disorganized, causing skeletal muscle hypoplasia and perinatal lethality. Transcriptome analysis demonstrated dramatic dysregulation of actin genes in MRTF dKO mice, highlighting the importance of MRTFs in actin cycling and myofibrillogenesis. MRTFs were also necessary for the survival of skeletal myoblasts and for the efficient formation of intact myotubes. Our findings reveal a central role for MRTFs in sarcomere formation during skeletal muscle development and point to the potential involvement of these transcriptional coactivators in skeletal myopathies.
2016-08-02 | GSE84063 | GEO
Project description:Skeletal muscle cells (myoblasts - human fetal cells from 17 week old embryo) Keywords: other
2005-09-01 | GSE3230 | GEO
Project description:NIH3T3 cell transiently transfected with myocardin-EGFP or EGFP. Transfection: Lipofectamine 2000 according to the manufacturers instructions (Invitrogen).
2013-11-15 | E-MEXP-3869 | biostudies-arrayexpress
Project description:Using microarray, we compared miRNAs expression profiles of MDA-MB-231 cells transfected with myocardin and empty vector (pcDNA3.1) and found that 25 miRNAs were significantly changed in myocardin-transfected groups (17 up-regulated and 9 down-regulated miRNAs). Moreover, we showed that 18 of 25 miRNAs significantly regulated by myocardin were inhibited by ERM-NM-1 in MDA-MB-231 cells. In addition,through a microarray approach, we identify the subset of miRNAs modulated by ERM-NM-1 in MDA-MB-231 cells. Our results determined that ERM-NM-1 may function as tumor-promoter through down-regulating expression of 3 miRNAs (miR-26b, miR-146a and miR-331-3p) in MDA-MB-231 cells. There are 4 samples in this experiment (pcDNA3.1-transfected, myocardin-transfected, ERM-NM-1-transfected, myocardin plus ERM-NM-1 co-transfecteded groups) and each sample was replicated 3 times. The vector-pcDNA3.1 was used as control.
2014-10-01 | E-GEOD-44139 | biostudies-arrayexpress
Project description:ABSTRACT Aims Forced differentiation of non-muscle cells into heart muscle cells using cardiac transcription factors (cTFs) may constitute a novel strategy to accomplish myocardial regeneration. Methods We investigated the potential of the cTF myocardin to induce cardiomyocyte differentiation and compared the myocardin-induced gene expression program to that of fully differentiated cardiomyocytes using oligonucleotide microarray hybridizations, quantitative RT-PCR analyses and immunofluorescence microscopy. The experiments were performed in the recently described human cardiomyocytes progenitor cells (hCMPCs), which differentiate into fully functional cardiomyocytes upon stimulation with 5-azacytidine and transforming growth factor β1. Results and Conclusions Forced myocardin expression stimulated transcription of a surprisingly large repertoire of heart muscle-specific genes in hCMPCs but did not cause their differentiation into functional cardiomyocytes. Specifically, myocardin gene transfer did not stimulate the synthesis of several sarcomeric (regulatory) proteins and ion channel constituents. The heart and smooth muscle-enriched isoforms of myocardin stimulate equally well the transcription of many of their cardiomyocyte-specific and virtually all of their smooth muscle target genes. However, the heart muscle-enriched myocardin species is a much more potent transactivator of a subset of genes encoding mainly cardiomyocyte-specific myofibrillar components. This may explain the underestimation of myocardin's cardiomyogenic potential in previous studies utilizing the smooth muscle-enriched isoform of this cTF.
2008-07-15 | GSE12110 | GEO
Project description:GATA4 occupancy on the mouse genome of satellite cell-derived primary myoblasts. Proliferating myoblasts cultured in growth medium were immunoprecipitated with anti-GATA4 antibody or control IgG. Precipitated genomic DNAs were subjected to next generation sequencing.
2015-04-10 | GSE67703 | GEO
Project description:Gene are regulated by Myocardin
| PRJNA529790 | ENA