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Genome-wide analysis of 8-oxoguanine DNA glycosylase-1 after oxidative stress exposure

ABSTRACT: We report the application of ChIP-Sequencing for profiling genome-wide distribution of 8-oxoguanine DNA glycosylase1 (OGG1, a DNA base excision repair protein), after oxidative stress exposure mediated by glucose oxidase (GOx) of cells. By obtaining an average of over 18 million of total reads per sample and over 19.5 million of unique reads per sample from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of HEK293 cells. We performed gene ontology and functional pathway analysis of genes associated with peaks to identify regions of the genomes (e.g. promoter, introns, etc) where the peaks tend to occur. The results show that OGG1 is primarily associated with promoter regions in vicinity of transcription factor binding sites 5' of transcription start sites (TSS). This pattern of distribution occurs in spite of genome-wide oxidative modifications of guanines (primarily 8-oxoG). OGG1 increased significantly at regulatory regions of CXC-, CC- chemokines, cytokines and growth factors. In controls, the DNA was chromatin immunoprecipitated using antibody to NF-κB/RelA. As expected NF-κB was enriched on gene regulatory regions including those of proinflammatory,cell proliferation ones. These and other data derived from further analysis, suggest that OGG1 modulates gene expression in coordination with NF-κB.

ORGANISM(S): Homo sapiens

PROVIDER: GSE89017 | GEO | 2018/07/06

REPOSITORIES: GEO

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Genome-wide analysis of 8-oxoguanine DNA glycosylase-1

Project description:We report the application of ChIP-Sequencing for profiling genome-wide distribution of 8-oxoguanine DNA glycosylase (OGG1) which is a DNA base excision repair protein, after TNF exposure of cells. By obtaining an average of over 18 million of total reads per sample and over 19.5 million of unique reads per sample from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of HEK293 cells. We performed gene ontology and functional pathway analysis of genes associate with peaks, and identify regions of the genomes (e.g. promoter, introns, etc) where the peaks tend to occur. The results show that OGG1 is primarily associated with promoter regions in vicinity of transcription factor binding sites 5' of transcription start sites (TSS). This pattern of distribution occurs in spite of genome-wide oxidative modifications of guanine (primarily 8-oxoG). OGG1 increased highly significant (1e-09 to 1e-517) enrichment of 57 transcription factor binding sites including those for Sox(2, 3, 6, 10), RUNX, RUNX(1, 2), HOX(C, D), STAT(1, 3, 6), IRF(1 to 4), NF-κB. In controls, the DNA was chromatin immunoprecipitated using antibody to NF-κB/RelA. These and other data derived from further analysis, suggest that OGG1 modulates binding of transcription factors and gene expression.

2018-07-15 | GSE75562 | GEO

Genome-wide identification of enhancer domains in the healthy and post-stroke mouse cortices

Project description:We report the identification of enhancer domains in sham and stroke mouse cerebral cortices by high-throughput profiling of H3K27Ac chromatin modification. A total of 35.4, 28.8 and 29.6 million reads were generated from chromatin immunoprecipitated DNA from sham, stroke and pooled input samples. This resulted in 55,571 peaks in sham and 56,110 peaks in stroke samples representing 50408 and 51,292 active regions, respectively. These active regions represent putative enhancer domains.

2020-11-12 | GSE135480 | GEO

Genome-wide Analysis of Vitamin D Receptor Binding By ChIP-Seq

Project description:We used ChIP-Seq to identify the genomic locations bound by the vitamin D receptor (VDR) in two lymphoblastoid cell lines (LCLs) (CEPH individuals GM10855 and GM10861 from the International HapMap Project) before and after calcitriol treatment for 36 hours. Immunoprecipitated DNA was sequenced using the Illumina Genome Analyzer II. Sequence reads (35 bases; 10-19 million quality-filtered reads/sample) were aligned to the human genome (NCBI Build 36.3) using ELAND software. The number of unique alignments ranged from 7.73 million to 14.32 million. Peaks were called in the aligned sequence data using a model-based analysis of ChIP-Seq (MACS) and compared with sequenced sonicated and amplified input DNA. In the samples not treated with calcitriol, the number of peaks ranged from 468 to 4538 (median 975, mean 1587), while in the calcitriol-treated samples the number of peaks was between 2560 and 7244 (median 4546, mean 4560). 65-75% of peaks of untreated samples were in promoters, while only 24-50% of peaks of calcitirol-treated samples were in promoters. This study provides a comprehensive map of VDR binding in lymphoblastoid cell lines. The GM10855 and GM10861 cell lines were either stimulated for 36 hours with calcitriol or unstimulated, and crosslinked with formaldehyde to generate a snapshot of all protein-DNA interactions occurring in the nucleus at that particular point in time. Antibodies were then used to immunoprecipitate the VDR protein together with the crosslinked DNA fragments. Following reversal of crosslinks and digestion of protein, adaptors were ligated to immunoprecipitated DNA, and bridge PCR was used to generate clonally amplified amplicons before sequencing by synthesis using the Illumina Solexa Genome Analyzer.

2010-06-22 | E-GEOD-22484 | biostudies-arrayexpress

Rad21-mediated NF-κB signaling limits hematopoietic stem cell self-renewal in aging and inflammation

Project description:MTD project_description Inflammation and decreased stem cell function characterize organism aging, yet the relationship between these factors remains incompletely understood. This study shows that aged hematopoietic stem and progenitor cells exhibit increased ground-stage NF-κB activity, which enhances their responsiveness to undergo differentiation and loss of self-renewal in response to inflammation. The study identifies Rad21/cohesin as a critical mediator of NF-κB signals, by increasing chromatin accessibility of inter-/intra-genic and enhancer regions. Rad21/NF-κB are required for normal differentiation, but limit self-renewal of hematopoietic stem cells (HSCs) during aging and inflammation in an NF-κB dependent manner. HSCs from aged mice fail to downregulate Rad21/cohesin and inflammation/differentiation inducing signals in the resolution phase after acute inflammation. and The inhibition of cohesin/NF-κB is sufficient to revert the hypersensitivity of aged HSPCs to inflammation-induced differentiation. During aging, myeloid-biased HSCs with disrupted and naturally occurring reduced expression of Rad21/cohesin are increasingly selected over lymphoid-biased HSCs. Together, Rad21/cohesin mediated NF-κB signaling limits HSPC function during aging and selects for cohesin deficient HSCs with myeloid skewed differentiation.

2018-11-28 | PXD011537 | Pride

Genome-wide Analysis of Vitamin D Receptor Binding By ChIP-Seq

2010-06-22 | GSE22484 | GEO

Genome-wide maps of TET1 binding in mouse frontal cortex

Project description:With anti-TET1 immunoprecipitated chromatin from mouse frontal cortices, we generated TET1 binding maps with 4496 high-confidence peaks and approximately 90% of TET1 peaks were within intergenic regions.

2019-07-25 | GSE124671 | GEO

Genome-wide maps of EGR1 binding in mouse frontal cortex

Project description:With anti-EGR1 immunoprecipitated chromatin from mouse prefrontal cortices, we generated EGR1 binding maps with 12, 014 high-confidence peaks. Approximately 81% of EGR1 peaks were within genic regions or nearby promoters, and over 45% EGR1 peaks were in the proximal promoter regions within 1 kb from transcription starting sites.

2019-07-31 | GSE67482 | GEO

A pseudogene lncRNA at the interface of inflammation and anti-inflammatory therapeutics

Project description:Pseudogenes are thought to be inactive gene sequences, but recent evidence of extensive pseudogene transcription raised the question of potential function. Here we discover and characterize the sets of lncRNAs induced by inflammatory signaling via TNFα. TNFα regulates hundreds of lncRNAs, including 54 pseudogene lncRNAs, several of which show exquisitely selective expression in response to specific cytokines and microbial components in a NF-κB-dependent manner. Lethe, a pseudogene lncRNA, is selectively induced by proinflammatory cytokines via NF-κB or glucocorticoid receptor agonist, and functions in negative feedback signaling to NF-κB. Lethe interacts with NF-κB subunit RelA to inhibit RelA DNA binding and target gene activation. Lethe level decreases with organismal age, a physiological state associated with increased NF-κB activity. These findings suggest that expression of pseudogenes lncRNAs are actively regulated and constitute functional regulators of inflammatory signaling. RNA profiles of wild type (WT) MEFs treated with TNF-alpha were generated by deep sequencing using Illumina GAIIx. Examination of H3K4me3 histome modification in MEF.

2013-08-05 | E-GEOD-47494 | biostudies-arrayexpress

Activation and partial inactivation of NF-κB signaling lead to hypertension and chronic kidney disease

Project description:Activation of NF-κB-signalling is key in the pathogenesis of chronic kidney diseases (CKD). However, a certain level of NF-κB activity is necessary to enable tissue repair and hence maintain a healthy kidney. To investigate the relationship between activated and inactivated NF-κB signaling on the pathogenesis of CKD, mouse models of NF-κB partial inactivation (mutating cysteine at position 59 of the sixth exon on the NF-κB gene into alanine) and activation (mutating cysteine at position 59 of the sixth exon on the NF-κB gene into serine) were used. Blood pressure, serum creatinine and urinary albumin-to-creatinine-ratio markedly increased in NF-κB activated and inactivated mice compared to controls. PAS-, Masson trichrome-, and Sirius-Red-staining, as well as α-SMA immunofluorescence staining in kidneys of NF-κBC59A, and NF-κBC59S mice demonstrated kidney fibrosis in both models. Transmission electron microscopy indicated that the glomerular basement membrane was thicker in both NF-κBC59A and NF-κBC59S mice compared to wild-type mice. KEGG enrichment analysis of RNA sequencing data revealed that the PPAR pathway was most markedly upregulated in both mouse models. However, there were also differences such as fatty acid degradation, peroxisome and glutathione metabolism, and downregulation of retinol metabolism in NF-κBC59A mice with decreased NF-κB signaling, whereas cell adhesion molecules, fat digestion, and absorption were upregulated in mice with activated NF-κB signaling (NF-κBC59S mice). In conclusion, using mice models with primarily activated and partially inactivated NF-κB pathways suggests that there is an apparently U-shaped relationship between kidney function as well as morphology and the activation of the NF-κB pathway.

2023-09-30 | GSE244099 | GEO

Assessment of host responses to ionizing radiation

Project description:The aim of this study was to analyze the host responses to ionizing radiation by nuclear factor-κB (NF-κB) bioluminescence imaging-guided transcriptomic tool. Transgenic mice, carrying the NF-κB-driven luciferase gene, were exposed to a single dose of 8.5 Gy total-body irradiation. In vivo imaging showed that a maximal NF-κB-dependent bioluminescent intensity was observed at 3 h after irradiation and ex vivo imaging showed that liver, intestine, and brain displayed strong NF-κB activations. Microarray analysis of these organs showed that irradiation altered gene expression signatures in an organ-specific manner. Pathway analysis showed that pathways associated with metabolism and immune system were altered primarily in liver and intestine. the upregulation of fatty acid binding protein 4, serum amyloid A2, and serum amyloid A3, which are participated in both inflammation and lipid metabolism, suggesting that irradiation might affect the cross pathways of metabolism and inflammation. Moreover, The upregulation of chemokine (CC-motif) ligand 5, chemokine (CC-motif) ligand 20, and Jagged 1 genes suggested that these genes might contribute to the radiation enteropathy. Male transgenic mice (6 to 8 weeks old) were exposed to a single dose of whole-body X-rays generated at 6 MV (Clinac® 21EX medical linear accelerator, Varian, Palo Alto, CA, USA) and at a dose rate of 4 Gy/min. Mice were imaged at 0 h, 1 h, 3 h, 9 h, 24 h, 48 h, or 72 h, or on 7 d or 14 d after irradiation with 8.5 Gy. RNAs were extracted at 3 h after irradiation.

2012-01-01 | E-GEOD-25208 | biostudies-arrayexpress

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