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

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

PROVIDER: PRJNA562688 | 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

Project description:Nickel induced transcriptional changes persist post exposure through epigenetic reprograming

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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.

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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 (ChIP-seq & RNA-seq datasets)

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

| PRJNA579383 | ENA

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 changes persist post exposure through epigenetic reprogramming.

Project description:BACKGROUND:Nickel 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. RESULTS:To 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. CONCLUSION:Our 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.

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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

Gene expression profile of nickel-stimulated HUVEC

Project description:Nickel compounds, important carcinogens and prime inducers of contact allergy in humans, are potent activators of endothelial cells (ECs). To elucidate the signaling pathways mediating the cellular responses to nickel we performed Affymetrix gene profiling of human primary ECs. Keywords: stress response

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Nickel Chloride (NiCl2) effect on human T cells from whole blood

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Project description:The goal of this study was to produce a reference transcriptome for the nickel hyperaccumulator Leucocroton havanensis endemic from Cuba and use this transcriptome as a reference to identify genes responding to the presence or the absence of nickel in both roots and shoots of this species

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