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Nickel induced transcriptional changes persist post exposure through epigenetic reprograming

ABSTRACT: Nickel induced transcriptional changes persist post exposure through epigenetic reprograming

PROVIDER: PRJNA579381 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10030341.fastq.gz	Fastqsanger.gz
	SRR10030342.fastq.gz	Fastqsanger.gz
	SRR10030343.fastq.gz	Fastqsanger.gz
	SRR10030344.fastq.gz	Fastqsanger.gz
	SRR10030345.fastq.gz	Fastqsanger.gz

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Nickel induced transcriptional changes persist post exposure through epigenetic reprograming (RNA-seq dataset)

Project description:Nickel induced transcriptional changes persist post exposure through epigenetic reprograming (RNA-seq dataset)

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Nickel induced transcriptional changes persist post exposure through epigenetic reprograming (ChIP-seq & RNA-seq datasets)

Project description:Nickel induced transcriptional changes persist post exposure through epigenetic reprograming (ChIP-seq & RNA-seq datasets)

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Nickel induced transcriptional changes persist post exposure through epigenetic reprograming (RNA-seq dataset)

Project description:Nickel is an occupational and environmental toxicant associated with a number of diseases. Our earlier studies showed that Ni-induced alterations to global gene expression persist even after the termination of exposure. A number of earlier studies suggest epigenome as a target of Ni. However, the genome wide dynamics of epigenetic modifications that potentially drive Ni-induced long-term transcriptional changes remain elusive.

2019-12-20 | GSE136558 | GEO

Nickel induced transcriptional changes persist post exposure through epigenetic reprograming (ChIP-seq & RNA-seq datasets)

2019-12-20 | GSE139355 | GEO

Nickel induced transcriptional changes persist post exposure through epigenetic reprograming

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-12-20 | GSE139356 | GEO

Nickel-induced transcriptional memory in lung epithelial cells promotes interferon signaling upon nicotine exposure

Project description:Nickel is an environmental toxicant prevalent in the atmosphere. Nickel exposure is associated with a multitude of human health hazards including chronic respiratory ailments and lung and nasal cancers. Our earlier studies on nickel exposure in lung cells showed that a majority of the gene expression changes caused by nickel exposure persisted even after termination of exposure (nickel-washed-out cells (NiW)). In this study, we wanted to examine the impact of a secondary toxicant exposure on the nickel-washed-out (NiW) cells as compared to the cells that were never exposed to nickel. To accomplish this, we exposed the untreated control cells (UT) and the nickel-washed-out cells (NiW) to multiple doses of nicotine (NTE). RNA-Seq analysis showed that the exposure of NiW cells to nicotine (NiW-NTE) caused unique gene expression changes that were markedly different from the gene expression changes caused by nicotine exposure of UT cells, which were never exposed to nickel. Analysis of the differentially expressed genes using Reactome Pathway analysis predicted interferon signaling only in the NiW-NTE cells. Upstream Regulator Analysis (URA) predicted STAT-1, a transcription factor that mediates cellular response to interferons, as the top potential upstream regulator in the NiW-NTE cells. Furthermore, chromatin immunoprecipitation (ChIP) analysis revealed increased STAT-1 binding at the promoters of genes associated with interferon signaling in NiW-NTE cells. Aberrant STAT-1 activation has been shown to promote carcinogenesis and interferon signaling promotes pathogenesis of autoimmune disease. Therefore, our results suggest that the epigenetic and transcriptional memory of the cells from the previous nickel exposure could negatively influence the outcome of secondary exposure to nicotine.

2023-11-11 | GSE242791 | GEO

Nickel-induced transcriptional changes persist post exposure through epigenetic reprogramming.

Project description:BackgroundNickel is an occupational and environmental toxicant associated with a number of diseases in humans including pulmonary fibrosis, bronchitis and lung and nasal cancers. Our earlier studies showed that the nickel-exposure-induced genome-wide transcriptional changes, which persist even after the termination of exposure may underlie nickel pathogenesis. However, the mechanisms that drive nickel-induced persistent changes to the transcriptome remain elusive.ResultsTo elucidate the mechanisms that underlie nickel-induced long-term transcriptional changes, in this study, we examined the transcriptome and the epigenome of human lung epithelial cells during nickel exposure and after the termination of exposure. We identified two categories of persistently differentially expressed genes: (i) the genes that were differentially expressed during nickel exposure; and (ii) the genes that were differentially expressed only after the termination of exposure. Interestingly, > 85% of the nickel-induced gene expression changes occurred only after the termination of exposure. We also found extensive genome-wide alterations to the activating histone modification, H3K4me3, after the termination of nickel exposure, which coincided with the post-exposure gene expression changes. In addition, we found significant post-exposure alterations to the repressive histone modification, H3K27me3.ConclusionOur results suggest that while modest first wave of transcriptional changes occurred during nickel exposure, extensive transcriptional changes occurred during a second wave of transcription for which removal of nickel ions was essential. By uncovering a new category of transcriptional and epigenetic changes, which occur only after the termination of exposure, this study provides a novel understanding of the long-term deleterious consequences of nickel exposure on human health.

| S-EPMC6921556 | biostudies-literature

Exposure to Nickel, Chromium, or Cadmium Causes Distinct Changes in the Gene Expression Patterns of a Rat Liver Derived Cell Line

Project description:Many heavy metals, including nickel (Ni), cadmium (Cd), and chromium (Cr) are toxic industrial chemicals with an exposure risk in both occupational and environmental settings that may cause harmful outcomes. While these substances are known to produce adverse health effects leading to disease or health problems, the detailed mechanisms remain unclear. To elucidate the processes involved in the of toxicity of nickel, cadmium, and chromium at the molecular level and to perform a comparative analysis, H4-II-E-C3 rat liver-derived cell lines were treated with soluble salts of each metal using concentrations derived from viability assays, and gene expression patterns were determined with DNA microarrays. We identified both common and unique biological responses to exposure to the three metals. Nickel, cadmium, chromium all induced oxidative stress with both similar and unique genes and pathways responding to this stress. Although all three metals are known to be genotoxic, evidence for DNA damage in our study only exists in response to chromium. Nickel induced a hypoxic response as well as inducing genes involved in chromatin structure, perhaps by replacing iron in key proteins. Cadmium distinctly perturbed genes related to endoplasmic reticulum stress and invoked the unfolded protein response leading to apoptosis. With these studies, we have completed the first gene expression comparative analysis of nickel, cadmium, and chromium in H4-II-E-C3 cells.

2011-08-19 | GSE31503 | GEO

Exposure to Nickel, Chromium, or Cadmium Causes Distinct Changes in the Gene Expression Patterns of a Rat Liver Derived Cell Line

2011-08-18 | E-GEOD-31503 | biostudies-arrayexpress

Gene expression of PBMC of chinese nickel refinery workers when compared to the gene expression profile of PBMCs from referent subjects

Project description:Up to date the studies examining the gene expression profiles in response to exposure to nickel compounds have only been conducted using in vitro tissue culture systems. Here, we have compared the gene expression profiles in peripheral blood mononuclear cells (PMCs) of eight nickel refinery workers in Jinchang, China to the expression profiles of referent subjects with only environmental exposure. PBMC RNA was collected from eight nickel refinery workers in China and ten reference subjects with only environmental exposure to nickel. PBMC RNA was labeled and hybridized to Affymetrix Genechip arrays 2.0. Gene expression profiles between nickel refinery workers and referent subjects was compared.

2012-08-28 | E-GEOD-40392 | biostudies-arrayexpress

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