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Myocardin-like Protein (MKL)-2 Regulates TGF-β Signaling in Embryonic Stem Cells and the Developing Vasculature

ABSTRACT: Signal transduction from the extracellular matrix to the arterial wall plays a critical role during development of the vasculature. We now report the discovery of a Myocardin-like Protein (MKL)2/TGF-β signaling pathway that is required for maturation and stabilization of the vasculature. Mkl2-/- null embryos exhibit profound derangements in the tunica media leading to aneurismal dilation, dissection and hemorrhage. TGFβ expression, signaling and TGF-β-regulated genes are down-regulated in Mkl2-/- ES cells and in the vasculature of Mkl2-/- embryos. Transcription of Tgfβ2 is activated via binding of a MKL 2/SRF complex to a conserved CArG element in the Tgfβ2 promoter. In this data set we include expression data from wild type and Mkl2-/- ES cells A total of 5 samples with mRNA of sufficient quality were analyzed. Samples consisted of mRNA from independent cell culture of 2 wild-type and 3 Mkl2-/- undifferentiated Embryonic Stem Cells

ORGANISM(S): Mus musculus

SUBMITTER: Nina Bowens

PROVIDER: E-GEOD-38316 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Myocardin-like Protein (MKL)-2 Regulates TGF-β Signaling in Embryonic Stem Cells and the Developing Vasculature

Project description:Signal transduction from the extracellular matrix to the arterial wall plays a critical role during development of the vasculature. We now report the discovery of a Myocardin-like Protein (MKL)2/TGF-β signaling pathway that is required for maturation and stabilization of the vasculature. Mkl2-/- null embryos exhibit profound derangements in the tunica media leading to aneurismal dilation, dissection and hemorrhage. TGFβ expression, signaling and TGF-β-regulated genes are down-regulated in Mkl2-/- ES cells and in the vasculature of Mkl2-/- embryos. Transcription of Tgfβ2 is activated via binding of a MKL 2/SRF complex to a conserved CArG element in the Tgfβ2 promoter. In this data set we include expression data from wild type and Mkl2-/- ES cells

2012-06-01 | GSE38316 | GEO

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

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

Transcription profiling of human skeletal myoblasts misexpressing myocardin

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

Gene are regulated by Myocardin

Project description:Gene are regulated by Myocardin

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Expression data from undifferentiated and differentiated mouse female ES cells PGK12.1

Project description:Affymetrix 430 2.0 mouse arrays were used for expression analyses in undifferentiated and differentiated PGK12.1 ES cells. We found that the X:autosome expression ratios calculated from the mean expression values of X-linked and autosomal genes from microarrays was ~1.4 in undifferentiated female ES cells and then decreased to 1.2 in PGK12.1 cells after 15-day embryoid body differentiation. Thus, a substantial level of X upregulation is already evident in these ES cells prior to differentiation. Our findings based on Affymetrix expression arrays are consistent with microarray analysis from other labs and our RNA-seq analysis of mouse female PGK12.1 ES cells. Mouse female ES cells PGK12.1 were differentiated by the EB (embryoid body) differentiation protocol. The presence of two active X chromosomes in undifferentiated female ES cells and one active X in 15-day differentiated cells was verified by Xist RNA FISH. Total RNA was prepared from undifferentiated and 15-day differentiated PGK12.1 and was used for expression array analyses to examine exprssion of the X chromosome during differentiation.

2013-02-15 | E-GEOD-44251 | 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.

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Expression data from mouse ES cells after control RNAi (scramble siRNAs) or RNAi specific for Kdm6a treatment.

Project description:To address the functional role of KDM6A in the regulation of Rhox genes, male and female mouse ES cells were transfected with a mixture of three small interfering RNA duplexes, each of which targets a different region of Kdm6a mRNA. We found that Kdm6a knockdown in mouse ES cells caused a decrease in expression of a subset of Rhox genes, Rhox6 and 9. Furthermore, Rhox6 and 9 expression was decreased in female ES cells but not male ES cells indicating that KDM6A regulates Rhox gene expression in a sexually dimorphic manner. Mouse ES cells were treated by Invitrogen scramble siRNA duplexes or specific siRNA duplexes and used for RNA extraction and hybridization on Affymetrix microarrays. Four RNA samples from two independent double-RNAi treatments and two single-RNAi treatment in undifferentiated female ES cells PGK12.1, and RNA samples from two single-RNAi treatments in undifferentiated male ES cells WD44 were assayed for expression changes by arrays.

2013-03-13 | E-GEOD-45034 | biostudies-arrayexpress

Mus musculus

Project description:Myocardin-like Protein (MKL)-2 Regulates TGF-β Signaling in Embryonic Stem Cells and the Developing Vasculature

| PRJNA167808 | ENA

Chip-seq of H3 in murine embryonic stem cells, myotubes and pro-B cells.

Project description:Nucleosome remodeling results in loss of histone occupancy. To gain insight into variations in H3 occupancy in different murine cell types, chromatin immunoprecipitation coupled with massive parallel sequencing (ChIP-seq) was performed to determine genome wide occupancy of H3 in ES cells, myotubes and pro-B cells. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. ChIP was performed using an antibody against total H3 in murine ES cells in normal culture conditions, murine ES cells treated with the TGF-beta inhibitor (SB431542, 10uM) for 24 hours, myotubes differentiated for 48 hours and pro-B cells under normal culture conditions.

2010-08-31 | E-GEOD-23830 | biostudies-arrayexpress

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