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Expression data from HUVEC adenovirally overexpressing MEF2C

ABSTRACT: The transcription factor MEF2C is specifically induced by VEGF in endothelial cells. To delineate target genes of MEF2C in endothelial cells, which might be important during angiogenesis also, MEF2C was overexpressed adenovirally in human umbilical vein endothelial cells (HUVECs) over a period of 8 to 32 hours. Expression data should be compared to control infected cells, to discriminate against virally induced genes, and should be further compared to HUVECs infected with an adenovirus encoding for a dominant-negative form of MEF2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE46279 | GEO | 2013/06/01

SECONDARY ACCESSION(S): PRJNA198513

REPOSITORIES: GEO

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Expression data from HUVEC adenovirally overexpressing MEF2C

Project description:The transcription factor MEF2C is specifically induced by VEGF in endothelial cells. To delineate target genes of MEF2C in endothelial cells, which might be important during angiogenesis also, MEF2C was overexpressed adenovirally in human umbilical vein endothelial cells (HUVECs) over a period of 8 to 32 hours. Expression data should be compared to control infected cells, to discriminate against virally induced genes, and should be further compared to HUVECs infected with an adenovirus encoding for a dominant-negative form of MEF2. HUVECs of the same batch, passage 3 were infected with Ad.con, Ad.MEF2C or Ad.DNMEF2 for 8, 16 or 32 hours for RNA extraction and hybridization on Affymetrix microarrays.

2013-06-01 | E-GEOD-46279 | biostudies-arrayexpress

Transcriptome profiling of murine aortic endothelium deleted for the transcription factor Mef2c

Project description:Laminar flow on endothelial cells in vitro activates MEF2 transcription factors to induce expression of atheroprotective genes. Here we sought to establish in vivo MEF2 functions in the endothelium through endothelial-specific deletion of Mef2c. Our results show that endothelial Mef2c regulates migration of vascular smooth muscle from the tunica media into the intima through fenestrations in the internal elastic lamina. Moreover, Mef2c regulates actin stress fiber formation in the endothelium. To investigate Mef2c-dependent targets in the endothelium, we perform transcriptome profiling on RNA isolated from the aortic endothelium with or without Mef2c deletion.

2017-05-31 | GSE97089 | GEO

Genome-wide maps of MEF2C and H3K27ac localization in HUVECs

Project description:MEF2C is one of the substantially expressed transcriptional factors in endothelial cells, but its genomic localization is unknown. This time, we established a new antibody for MEF2C, and performed ChIP-seq to identify MEF2C binding site in whole genome manner. H3K27Ac binding sites were also detected in the same way. We used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with or without pitavastatin for 4hours, we identified MEF2C and H3K27Ac binding regions.HUVECs were used within the first 6 passages. For MEF2C studies, HUVECs were cultivated in medium EGM2MV containing pitavastatin at a concentration of 1 ?M, and same concentration of DMSO was used as a control sample. For H3K27ac, HUVECs were starved for 16 hours and harvested without statin treatment.

2013-01-01 | E-GEOD-32644 | biostudies-arrayexpress

Role of MEF2C in the Endothelial Cells Derived from Human Induced Pluripotent Stem Cells

Project description:Human induced pluripotent stem cells (hiPSCs) not only provide an abundant source of vascular cells for potential therapeutic applications in vascular disease but also constitute an excellent model for understanding the mechanisms that regulate the differentiation and the functionality of vascular cells. Here, we reported that myocyte enhancer factor 2C (MEF2C) transcription factor, but not any other members of the MEF2 family, was robustly upregulated during the differentiation of vascular progenitors and endothelial cells (ECs) from hiPSCs. Vascular endothelial growth factors (VEGF) strongly induced MEF2C expression in endothelial lineage cells. The specific upregulation of MEF2C during the commitment of endothelial lineage was dependent on the extracellular signal regulated kinase (ERK). Moreover, knockdown of MEF2C with shRNA in hiPSCs did not affect the differentiation of ECs from these hiPSCs, but greatly reduced the migration and tube formation capacity of the hiPSC-derived ECs. Through a chromatin immunoprecipitation-sequencing, genome-wide RNA-sequencing, quantitative RT-PCR, and immunostaining analyses of the hiPSC-derived endothelial lineage cells with MEF2C inhibition or knockdown compared to control hiPSC-ECs, we identified TNF-related apoptosis inducing ligand (TRAIL) and transmembrane protein 100 (TMEM100) as novel targets of MEF2C. This study demonstrates an important role for MEF2C in regulating human EC functions and highlights MEF2C and its downstream effectors as potential targets to treat vascular malfunction-associated diseases.

2024-01-01 | GSE222083 | GEO

Gene expression analysis to identify Mef2c/d target genes in B-cell progenitors

Project description:The sequential activation of distinct developmental gene networks governs the ultimate identity of a cell, but the mechanisms by which downstream programs are activated are incompletely understood. The preB-cell receptor (preBCR) is an important checkpoint of B-cell development and essential for a preB-cell to traverse into an immature B-cell. Here, we show that activation of Mef2 transcription factors by preBCR is necessary for initiating the subsequent genetic network. We demonstrate that B-cell development is blocked at the preB-cell stage in mice deficient for Mef2c and Mef2d transcription factors and that preBCR signaling enhances the transcriptional activity of Mef2c/d through phosphorylation by the ERK5 mitogen activating kinase. This activation is instrumental in inducing KrÃ¼ppel-like factor 2 and several immediate early genes of the AP1 and Egr family. Finally, we show that Mef2 proteins cooperate with the products of their target genes (Irf4 and Egr2) to induce secondary waves of transcriptional regulation. Our findings uncover a novel role for Mef2c/d in coordinating the transcriptional network that promotes early B-cell development. RNA-seq experiments were performed from Mef2c/d knockout proB-cells versus control cells to identify genes regulated by Klf2

2015-12-14 | E-GEOD-73561 | biostudies-arrayexpress

DNA microarrays (time course) of MEFs transduced with SKO plus HDAC7 or MEF2C

Project description:Overexpression HDAC7 can enhance iPS efficiency in SKO by supressing MEF2 factors We used microarrays to identify changes induced by overexpression of HDAC7 or MEF2C. MEFs were transduced with SKO plus HDAC7 or MEF2C compared to SKO plus empty vector(Flag), GFP as controls. TRIZOL cell lysates were prepared from D6 and D10.

2011-08-17 | E-GEOD-23692 | biostudies-arrayexpress

DNA microarrays (time course) of MEFs transduced with SKO plus HDAC7 or MEF2C

Project description:Overexpression HDAC7 can enhance iPS efficiency in SKO by supressing MEF2 factors We used microarrays to identify changes induced by overexpression of HDAC7 or MEF2C.

2011-08-18 | GSE23692 | GEO

Genome-wide mapping of Mef2c-bound sites in early B-cell progenitors

Project description:The sequential activation of distinct developmental gene networks governs the ultimate identity of a cell, but the mechanisms by which downstream programs are activated are incompletely understood. The preB-cell receptor (preBCR) is an important checkpoint of B-cell development and essential for a preB-cell to traverse into an immature B-cell. Here, we show that activation of Mef2 transcription factors by preBCR is necessary for initiating the subsequent genetic network. We demonstrate that B-cell development is blocked at the preB-cell stage in mice deficient for Mef2c and Mef2d transcription factors and that preBCR signaling enhances the transcriptional activity of Mef2c/d through phosphorylation by the ERK5 mitogen activating kinase. This activation is instrumental in inducing KrÃ¼ppel-like factor 2 and several immediate early genes of the AP1 and Egr family. Finally, we show that Mef2 proteins cooperate with the products of their target genes (Irf4 and Egr2) to induce secondary waves of transcriptional regulation. Our findings uncover a novel role for Mef2c/d in coordinating the transcriptional network that promotes early B-cell development. ChIP-seq experiments were performed in the proB-cell line BMiFLT3(15-3) to identify Mef2c-bound sites in early B-cell progenitors.

2015-12-14 | E-GEOD-73453 | biostudies-arrayexpress

MEF2C Protein Isoform Transition to a Repressor Variant is Linked to Development of Heart Failure

Project description:The transcription factor MEF2C has been implicated in the pathogenesis of cardiac remodeling and heart failure. The underlying mechanisms of the MEF2C detrimental effects still remain elusive. MEF2C is unique among the MEF2 family in that alternative splice acceptors in the last exon give forms that include or exclude a short domain, which has an inhibitory effect on the MEF2C activity. Objective: To identify if MEF2Cγ+ repressor variant has a role in the cardiac detrimental effects of MEF2C. Conclusions: We conclude that upregulation of MEF2Cγ+ in adult hearts causes cardiac pathogenic features through dysregulation of cell cycle and dedifferentiation of cardiomyocytes.

2020-01-22 | GSE99748 | GEO

Bone marrow-induced Mef2c deficiency delays B cell development and alters the expression of key B cell regulatory proteins

Project description:The Mef2 family transcriptional regulator Mef2c is highly expressed in maturing bone marrow and peripheral mature B cells. To evaluate the role of this transcription factor in B cell development, we generated a B cell specific conditional deletion of Mef2c using the Mb-1-Cre transgene that is expressed during the early stages of immunoglobulin rearrangement. Young mice possessing this defect demonstrated a significant impairment in B cell numbers in bone marrow and spleen. This phenotype was evident in all B cell subsets; however, as the animals mature, the deficit in the peripheral mature B cell compartments was overcome. The absence of Mef2c in mature B cells led to unique CD23+ and CD23- subsets that were evident in Mef2c KO primary samples as well as cultured, differentiated B cells but not in WT cell populations. Genome wide expression analysis of immature and mature B cells lacking Mef2c indicated altered expression for a number of key regulatory proteins for B cell function including Ciita, CD23, Cr1/Cr2, and Tnfsf4. Chromatin immunoprecipitation analysis confirmed Mef2c binding to the promoters of these genes indicating a direct link between the presence (or absence) of Mef2c and altered transcriptional control in mature B cells. Four samples are submitted.

2012-05-31 | E-GEOD-34210 | biostudies-arrayexpress

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