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Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (ChIP-seq)

ABSTRACT: We report that hyperglycemia-mediated induction of genes and pathways associated to endothelial dysfunction occur through modulation of acetylated H3K9/K14 inversely correlated with methyl-CpG content. Examination of H3K9/K14 histone acetylation and DNA methylation in hyperglycemic conditions.

ORGANISM(S): Homo sapiens

SUBMITTER: Assam El-Osta

PROVIDER: E-GEOD-29251 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells.

Pirola Luciano L Balcerczyk Aneta A Tothill Richard W RW Haviv Izhak I Kaspi Antony A Lunke Sebastian S Ziemann Mark M Karagiannis Tom T Tonna Stephen S Kowalczyk Adam A Beresford-Smith Bryan B Macintyre Geoff G Kelong Ma M Hongyu Zhang Z Zhu Jingde J El-Osta Assam A El-Osta Assam A

Genome research 20110902 10

Emerging evidence suggests that poor glycemic control mediates post-translational modifications to the H3 histone tail. We are only beginning to understand the dynamic role of some of the diverse epigenetic changes mediated by hyperglycemia at single loci, yet elevated glucose levels are thought to regulate genome-wide changes, and this still remains poorly understood. In this article we describe genome-wide histone H3K9/K14 hyperacetylation and DNA methylation maps conferred by hyperglycemia in ...[more]

PMID: 21890681

Similar Datasets

Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (gene expression)

Project description:We report that hyperglycemia-mediated induction of genes and pathways associated to endothelial dysfunction occur through modulation of acetylated H3K9/K14 inversely correlated with methyl-CpG content. Examination of H3K9/K14 histone acetylation and DNA methylation in hyperglycemic conditions. see GSE29251 for histone acetylation and DNA methylation

2011-07-19 | E-GEOD-30780 | biostudies-arrayexpress

Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (gene expression)

2011-07-20 | GSE30780 | GEO

Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (ChIP-seq)

2011-06-01 | GSE29251 | GEO

Genome-wide profiling of H3K9/K14 Acetylation and H3K27 trimethylation at promoters in the human lung embryonic fibroblast cell line MRC5

Project description:Genome-wide profiling of H3K9/K14 Acetylation and H3K27 trimethylation at promoters in the human lung embryonic fibroblast cell line MRC5

2013-11-11 | E-MTAB-2004 | biostudies-arrayexpress

Hyperglycemia potentiates brain susceptibility to lipopolysaccharide-induced neuroinflammation by astrocytes reprogramming

Project description:Hyperglycemia has been shown to modulate the immune response of peripheral immune cells and organs, but the impact of hyperglycemia on neuroinflammation within the brain remains elusive. In the present study, we provide evidences that streptozotocin (STZ)-induced hyperglycemic condition in mice drives a phenotypic switch of brain astrocytes to a proinflammatory and neurotoxic state, and increases brain vulnerability to mild peripheral inflammation. In particular, we found that hyperglycemia led to a significant increase in the astrocyte proliferation as determined by flow cytometric and immunohistochemical analyses of mouse brain. Transcriptomic analysis of isolated astrocytes from Aldh1l1CreER;tdTomato mice revealed that peripheral STZ injection induced astrocyte reprogramming into proliferative, proinflammatory and neurotoxic phenotype. Additionally, STZ-induced hyperglycemic condition significantly enhanced the infiltration of circulating myeloid cells into the brain and the disruption of blood-brain barrier in response to mild lipopolysaccharide (LPS) administration. Systemic hyperglycemia did not alter the intensity and sensitivity of peripheral inflammation in mice to LPS challenge, but increased the inflammatory potential of brain microglia. Furthermore, hyperglycemic mice exhibited a significant impairment in cognitive function after mild LPS administration compared to normoglycemic mice as determined by novel object recognition and Y-maze tasks. Taken together, these results demonstrate that hyperglycemia directly induces astrocyte reprogramming towards a proliferative and proinflammatory phenotype, which potentiates mild LPS-triggered inflammation within brain parenchymal regions.

2024-06-05 | GSE247033 | GEO

Vascular histone deacetylation by pharmacological HDAC inhibition [TSA, ChIP-seq]

Project description:HDAC inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. Often studied at single loci, increased histone acetylation is the paradigmatic mechanism of action, however, little is known of the extent of genome-wide changes of the mammalian genome when stimulated by the hydroxamic acids, TSA and SAHA. In primary human vascular endothelial cells we map the chromatin modifications, histone H3 acetylation of lysine 9 and 14 (H3K9/14ac) using chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq). Since acetylation mediated gene expression is often associated with modification of other lysine residues we also examined H3K4me3 and H3K9me3 as well as changes in CpG methylation (CpG-seq). Genome-wide mRNA sequencing indicates the differential expression of about 30% of genes, with almost equal numbers being up- and down- regulated. We observe deacetylation conferred by TSA and SAHA that are associated with decreased gene expression. Histone deacetylation is associated with the loss of p300/CBP binding at gene promoters. This study provides an important framework for HDAC inhibitor function in vascular biology and a comprehensive description of genome-wide deacetylation. HAEC ChIP-seq profiles for 3 histone marks of TSA treated and control samples were generated by deep sequencing, in triplicate, using Illumina GAIIx.

2014-02-23 | E-GEOD-37377 | biostudies-arrayexpress

Vascular histone deacetylation by pharmacological HDAC inhibition [SAHA, ChIP-seq]

Project description:HDAC inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. Often studied at single loci, increased histone acetylation is the paradigmatic mechanism of action, however, little is known of the extent of genome-wide changes of the mammalian genome when stimulated by the hydroxamic acids, TSA and SAHA. In primary human vascular endothelial cells we map the chromatin modifications, histone H3 acetylation of lysine 9 and 14 (H3K9/14ac) using chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq). Since acetylation mediated gene expression is often associated with modification of other lysine residues we also examined H3K4me3 and H3K9me3 as well as changes in CpG methylation (CpG-seq). Genome-wide mRNA sequencing indicates the differential expression of about 30% of genes, with almost equal numbers being up- and down- regulated. We observe deacetylation conferred by TSA and SAHA that are associated with decreased gene expression. Histone deacetylation is associated with the loss of p300/CBP binding at gene promoters. This study provides an important framework for HDAC inhibitor function in vascular biology and a comprehensive description of genome-wide deacetylation. HAEC ChIP-seq profiles for 3 histone marks of SAHA treated and control samples were generated by deep sequencing, in triplicate, using Illumina GAIIx.

2014-02-23 | E-GEOD-54909 | biostudies-arrayexpress

Histone H3K9 and H3K14 acetylation mark active enhancers and promoters together with bivalent promoters in mouse embryonic stem cells

Project description:Transcription regulation in pluripotent embryonic stem (ES) cells is a complex process that involves multitude of regulatory layers, one of which is post-translational modification of histones. Here we have investigated the genome-wide occurrence of two histone marks, acetylation of histone H3K9 and K14 (H3K9ac and H3K14ac), in mouse ES cells. We demonstrate genome-wide that H3K9ac and H3K14ac show very high correlation. Examination of H3K9ac and H3K14ac in mES cells

2012-10-01 | E-GEOD-31284 | biostudies-arrayexpress

Hyperglycemia promotes an aggressive phenotype in breast cancer cells

Project description:Diabetes and breast cancer are common diseases with a major impact on the health sector in Mexico and worldwide. Epidemiological and experimental works support the link between type 2 diabetes and breast cancer; these data support that insulin resistance, hyperglycemia, hyperinsulinemia, and elevated levels of IGF-1 in patients with type II diabetes mellitus promote growth and invasiveness of tumor cells. The aim of the present work was to determine, by microarray, the mechanisms of action and signaling of a hyperglycemic microenvironment in the cell line (MDA-MB-231) and its effect to treatment with cisplatin (CCP). MDA-MB-231 breast cancer cells were cultured in DMEM medium, supplemented with 10% fetal bovine serum and antibiotics at 5% CO2, at 37 ˚C. We proceeded to extract total RNA for the analysis of microarrays under LG (low glucose) and HG (high glucose) conditions; for the cDNA synthesis, it was labeled with dUTP-Cy3 or dUTP-Cy5 fluorophores, using a CyScribe Firs-Strand cDNA kit. The analysis was carried out through the KEGG pathways program; some bioenergetic metabolism processes (glycolysis, biosynthesis of purines and pyrimidines, and metabolism of glycerol phospholipids) were found altered, which fulfill the feedback function to the cellular microenvironment, activating some signaling processes, such as the Hippo route, PI3K-Akt, Jak-STAT, MAPK, Ras, Wnt/β-catenin, apoptosis, and favoring an aggressive phenotype and drug resistance in a hyperglycemic microenvironment. The microarray analysis was validated by qRT-PCr of the tetraspanin and Frizzled genes.

2019-08-24 | GSE136277 | GEO

Rice NSF45K microarray experiment to explain Xa21, NH1 and NRR mediated defense responses in rice

Project description:Rice Xa21 resistance gene, which encodes a protein with predicted leucine-rich repeat (LRR), transmembrane, juxtamembrane, and intracellular kinase domains, conferred immunity to diverse strains of Xanthomonas oryzae pv. oryzae (Xoo). We generated Xa21 plant on TP309 background (Oryza Sativa Japonica). Systemic Acquired Resistance (SAR) in plants confers durable broad-spectrum resistance to pathogens and requires a phytohormone, salicylic acid (SA). Arabidopsis NPR1/NIM1 is a key regulator of the SAR response. Recently, we found that rice NPR1 homolog 1 (NH1) mediated enhanced resistance responses for Xoo (Chern et al., 2005b). We further investigated relating pathways in rice by identifying proteins that interact with NH1. One of them, constitutive over-expression of NH1 mediated negative regulator of resistance (NRR) gene caused enhanced susceptibility to Xoo , indicating that this gene product negatively affects to basal resistance response (Chern et al., 2005a). To dissect defense responses for rice bacterial blight pathogen, we planed microarray using two resistant mutant named with Xa21-TP309, NH1ox and one super-susceptible mutant (NRRox) before pathogen inoculation and one day post pathogen inoculation. Keywords: Biotic stress response Two or Three-condition experiment, NH1ox vs wild type control (LG) at two durations of Xoo inoculation (0d and 1d); NRRox vs wild type control (LG) at two durations of Xoo inoculation (0d and 1d); and Xa21vs wild type control (TP309) at three durations of Xoo inoculation (0d,1d and 2d);. Biological replicates: 2 or 4, independently grown and harvested.

2011-02-28 | E-GEOD-22112 | biostudies-arrayexpress

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