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ChIP-chip of BMP2 or control treated human pulmonary artery endothelial cells with anti-beta-catenin or anti-ppar-gamma antibodies on promoter regions

ABSTRACT: Reduced bone morphogenetic protein receptor (BMPR)2 expression in patients with pulmonary arterial (PA) hypertension (PAH), can impair PA endothelial cell (EC) function. We now characterize, in human PAECs, a novel BMPR2-mediated transcriptionally active complex between peroxisome proliferator-activated receptor (PPAR) gamma and beta-catenin (BC), and show that disruption of this complex impairs BMP mediated HPAEC survival. Using whole genome wide ChIP-Chip promoter analysis we delineate PPARG-BC dependent transcription of target genes that include apelin. Comparison of ppar-gamma and beta-catenin occupancy on promoter regions from human pulmonary artery endothelial cells after either treatment with BMP2 or control. A total of 8 samples were created using NimbleGen human HG18 promoter arrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Molong Li

PROVIDER: E-GEOD-29489 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ChIP-chip of BMP2 or control treated human pulmonary artery endothelial cells with anti-beta-catenin or anti-ppar-gamma antibodies on promoter regions

Project description:Reduced bone morphogenetic protein receptor (BMPR)2 expression in patients with pulmonary arterial (PA) hypertension (PAH), can impair PA endothelial cell (EC) function. We now characterize, in human PAECs, a novel BMPR2-mediated transcriptionally active complex between peroxisome proliferator-activated receptor (PPAR) gamma and beta-catenin (BC), and show that disruption of this complex impairs BMP mediated HPAEC survival. Using whole genome wide ChIP-Chip promoter analysis we delineate PPARG-BC dependent transcription of target genes that include apelin.

2011-05-25 | GSE29489 | GEO

Genome-wide analysis of human pulmonary artery endothelial cells after knockdown of either BMPRII or beta-catenin

Project description:Expression analysis of genes potentially regulated by BMPRII and beta-catenin. BMPRII has been linked as a genetic factor to the disease pulmonary arterial hypertension. Comparison of total mRNA obtained from human pulmonary artery endothelial cells treated with control, bone morphogentic protein receptor II, or beta-catenin siRNA

2010-11-06 | E-GEOD-18956 | biostudies-arrayexpress

Single cell atlas identifies lipid-processing and immunomodulatory endothelial cells in healthy and malignant breast

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Effects of Beta Catenin antagonist BC2059 in AML cells

Project description:To determine the global transcriptomic changes induced by treatment with the Beta Catenin antagonist BC2059 in AML cells The canonical WNT-β-catenin pathway is essential for self-renewal, growth and survival of AML stem/blast progenitor cells (BPCs). Deregulated WNT signaling inhibits degradation of β-catenin, causing increased nuclear translocation and co-factor activity of β-catenin with the transcriptional regulator TCF4/LEF1 in AML BPCs. Here, we determined the pre-clinical anti-AML activity of the anthraquinone oxime-analog BC2059 (BC), known to attenuate β-catenin levels. BC treatment disrupted the binding of β-catenin with the scaffold protein TBL1 (transducin β-like 1) and proteasomal degradation and decline in the nuclear levels of β-catenin. This was associated with reduced transcriptional activity of TCF4 and expression of its target genes, cyclin D1, c-Myc and survivin. BC treatment dose-dependently induced apoptosis of cultured and primary AML BPCs. Treatment with BC also significantly improved the median survival of immune-depleted mice engrafted with either cultured or primary AML BPCs exhibiting nuclear expression of β-catenin. Co-treatment with the pan-histone deacetylase inhibitor panobinostat and BC synergistically induced apoptosis of cultured and primary AML BPCs, including those expressing FLT3-ITD, as well as further significantly improved the survival of immune-depleted mice engrafted with primary AML BPCs. These findings underscore the promising pre-clinical activity and warrant further testing of BC against human AML, especially those expressing FLT3-ITD.

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PLD1 promotes tumor invasion by regulation of MMP-13 expression via phosphorylation of NF-kB in bladder cancer

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Histone H3K9 Methyltransferase G9a Represses PPAR? Expression and Adipogenesis [ChIP-Seq and RNA-Seq data]

Project description:PPAR? promotes adipogenesis while Wnt proteins inhibit adipogenesis. However, the mechanisms that control expression of these positive and negative master regulators of adipogenesis remain incompletely understood. By genome-wide histone methylation profiling in preadipocytes, we find that among gene loci encoding adipogenesis regulators, histone methyltransferase (HMT) G9a-mediated repressive epigenetic mark H3K9me2 is enriched on the entire PPAR? locus. H3K9me2 and G9a levels decrease during adipogenesis, which correlates inversely with induction of PPAR?. Removal of H3K9me2 by G9a deletion enhances chromatin opening and binding of adipogenic transcription factor C/EBP-beta to PPAR? promoter, which promotes PPAR? expression. Interestingly, G9a represses PPAR? expression in an HMT activity-dependent manner but facilitates Wnt10a expression independent of its enzymatic activity. Consistently, deletion of G9a or inhibiting G9a HMT activity promotes adipogenesis. Finally, deletion of G9a in mouse adipose tissues increases adipogenic gene expression and tissue weight. Thus, by inhibiting PPAR? expression and facilitating Wnt10a expression, G9a represses adipogenesis. Examination of 3 different histone modification changes in 3T3-L1 preadipocytes

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Identification of β-Catenin-Interacting Proteins in Nuclei of Aquaporin-2-Expressing Rat Collecting Duct Cells

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Chip-chip from Human Pulmonary Fibroblasts with H3K9me2 antibody

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2011-08-28 | E-GEOD-29381 | biostudies-arrayexpress

Homo sapiens

Project description:ChIP-chip of BMP2 or control treated human pulmonary artery endothelial cells with anti-beta-catenin or anti-ppar-gamma antibodies on promoter regions

| PRJNA141651 | ENA

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