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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human skeletal myoblasts misexpressing myocardin

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: G Teg Pipes

PROVIDER: E-GEOD-3378 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Stem cells and their derivatives can bypass the requirement of myocardin for smooth muscle gene expression.

Pipes G C Teg GC Sinha Sanjay S Qi Xiaoxia X Zhu Chun-Hong CH Gallardo Teresa D TD Shelton John J Creemers Esther E EE Sutherland Lillian L Richardson James A JA Garry Daniel J DJ Wright Woodring E WE Owens Gary K GK Olson Eric N EN

Developmental biology 20051123 2

The Serum Response Factor (SRF) coactivator myocardin stimulates the transcription of multiple muscle genes during cardiac and smooth muscle development. Mouse embryos lacking myocardin die during the earliest stages of smooth muscle development and fail to express multiple smooth muscle marker genes in the embryonic dorsal aorta and other vascular structures. In this study, we used mutant embryonic stem cell lines to further define the role of myocardin in smooth muscle differentiation and vasc ...[more]

PMID: 16310178

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Effect of myocardin mis-expression in human skeletal myoblasts

Project description:transcriptional effects of mis-expression of full length (935) myocardin in growing human skeletal myoblasts Keywords: mis-expression of transcriptional co-activator

2005-10-27 | GSE3378 | GEO

Skeletal muscle myoblasts: GATA4-Wt, -KO, -OE; day 0, 3

Project description:Gene expression in satellite cell-derived primary myoblasts islolated from Gata4-loxP mice. Myoblasts were infected with nLacZ for control (Wt), Cre recombinase to knockout GATA4 (KO), or GATA4 expression vector to overexpress GATA4 (OE). Infected myoblasts were cultured in growth medium (day 0) then differentiated into myotubes in differentiation medium for 3 days (day 3).

2015-02-18 | GSE66016 | GEO

Skeletal muscle myoblasts: GATA4-Wt, -KO, -OE; day 0, 3

2015-02-18 | E-GEOD-66016 | 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

Homo sapiens

Project description:Effect of myocardin mis-expression in human skeletal myoblasts

| PRJNA93507 | ENA

2016-08-02 | GSE84063 | GEO

Embryonic Skeletal Myoblasts

Project description:Skeletal muscle cells (myoblasts - human fetal cells from 17 week old embryo) Keywords: other

2005-09-01 | GSE3230 | GEO

NIH3T3 transfected with myocardin

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

miRNAs were significantly regulated by myocardin and ERM-NM-1

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

Gene expression profiling of overexpression of myocardin

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

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