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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. 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Caterina Sturtzel

PROVIDER: E-GEOD-46279 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2013-06-01 | GSE46279 | GEO

Genome-wide maps of MEF2C and H3K27ac localization in HUVECs

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

bHLH transcription factor ATOH8 overexpression effect on endothelial cells: gain-of-function model [GOF]

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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.

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Genome-wide maps of MEF2C and H3K27ac localization in HUVECs

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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

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

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2012-04-10 | E-GEOD-34628 | biostudies-arrayexpress

Modifications of the composition of the hyphal outerlayer of Aspergillus fumigatus affects HUVEC inflammatory and immune response

Project description:Aspergillus fumigatus is an angioinvasive fungal pathogen and the main etiologic agent causing invasive aspergillosis. Upon contact with human umbilical vein endothelial cells (HUVECs), this fungus induces cellular injury, inflammatory response and a pro-thrombotic phenotype. The pathogen molecules involved in this processes are however still unknown. A. fumigatus hyphae have been shown to produce, both in vivo and in vitro, an extracellular matrix composed of galactomannan, galactosaminogalactan and α-(1,3)-glucan. The deletion of the UDP-Galp mutase results in a mutant with a very sticky phenotype, due to the increase in the galactosaminogalactan content in the cell surface. The overexpression of galactosaminogalactan in this mutant was confirmed by immunofluorescence microscopy with a monoclonal antibody. Interestingly, the adhesion of ∆ugm1 germlings to HUVECs was significantly higher in comparison to the wild type strain. The ∆ugm1 adhesion capacity was followed by an increment in the cytokine secretion and tissue factor expression by infected endothelial cells. Using a shotgun proteomic approach with label-free quantification, we were able to search and compare pathways regulated in endothelial cells challenged with A. fumigatus, wild type and ∆ugm1. The deletion of the UGM1 gene in A. fumigatus induced changes in the endothelial cell response, maily related to immune and stress responses. In addition, the purified urea soluble fraction of galactosaminogalactan was able to induce TNF-α secretion by HUVECs and also regulate coincident pathways identified in the mutant interaction condition. This work describes for the first time the impact of the modifications of the hyphal surface galactosaminogalactan on the endothelial cell responses to A. fumigatus.

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Global analysis of NFATc1 targets in human vascular endothelial cells

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2013-09-01 | E-GEOD-49426 | biostudies-arrayexpress

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