Ontology highlight
ABSTRACT:
PROVIDER: PRJNA801193 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17782947_1.fastq.gz | Fastqsanger.gz | |||
| SRR17782947_2.fastq.gz | Fastqsanger.gz | |||
| SRR17782948_1.fastq.gz | Fastqsanger.gz | |||
| SRR17782948_2.fastq.gz | Fastqsanger.gz | |||
| SRR17782949_1.fastq.gz | Fastqsanger.gz |
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Project description:Transcriptome analysis of the larvae of Protohermes xanthodes exposed to chlorpyrifos
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Project description:RNA-seq analysis of gestationally Cd-exposed hepatic transcriptome
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Project description:BACKGROUND: Cadmium is implicated in prostate carcinogenesis, but its oncogenic action remains unclear. OBJECTIVES: In this study we aimed to decipher changes in cell growth and the transcriptome in an immortalized human normal prostate epithelial cell line (NPrEC) following exposure to low-dose Cd. METHODS: Synchronized NPrEC cells were exposed to different doses of Cd and assayed for cell viability and cell-cycle progression. We investigated changes in transcriptome by global profiling and used Ingenuity Pathways Analysis software to develop propositions about functional connections among differentially expressed genes. A neutralizing antibody was used to negate the effect of Cd-induced up-regulation of tumor necrosis factor (TNF) in NPrEC cells. RESULTS: Exposure of NPrEC to 2.5 μM Cd enhanced cell viability and accelerated cell-cycle progression. Global expression profiling identified 48 genes that exhibited ≥ 1.5-fold changes in expression after 4, 8, 16, and 32 hr of Cd treatment. Pathway analyses inferred a functional connection among 35 of these genes in one major network, with TNF as the most prominent node. Fourteen of the 35 genes are related to TNF, and 11 exhibited an average of > 2-fold changes in gene expression. Real-time reverse transcriptase-polymerase chain reaction confirmed the up-regulation of 7 of the 11 genes (ADAM8, EDN1, IL8, IL24, IL13RA2, COX2/PTGS2, and SERPINB2) and uncovered a 28-fold transient increase in TNF expression in Cd-treated NPrEC cells. A TNF-neutralizing antibody effectively blocked Cd-induced elevations in the expression of these genes. CONCLUSIONS: Noncytotoxic, low-dose Cd has growth-promoting effects on NPrEC cells and induces transient overexpression of TNF, leading to up-regulation of genes with oncogenic and immunomodulation functions. KEY WORDS: carcinogenesis, cytokine, global expression profiling, heavy metals, immune response, inflammation, Ingenuity Pathway Analysis, knowledge-based analysis, prostate cancer.
2008-03-01 | GSE9951 | GEO
Project description:Gene expression can vary with the organisms' life stage. It is known that embryos can be more sensitive to toxicant exposure, as previously demonstrated for Enchytraeus crypticus (Oligochaeta) exposed to cadmium (Cd), known to cause embryotoxicity and hatching delay. It was shown that Ca enters embryos via the L-type Ca channels in the cocoon membrane, this being affected in Cd exposed embryos (Cd-Ca competition is well-known). In the present study, the embryotoxic mechanisms of Cd were studied via high-throughput gene expression for E. crypticus. Cocoons (1e2 days old), instead of the adult organism, were exposed in Cd spiked LUFA 2.2 soil during 1 day. Results showed that Cd affected Ca homeostasis which is implicated in several other molecular processes. Several of the major modulators of Cd toxicity (e.g., impaired gene expression, cell cycle arrest, DNA and mitochondrial damage) were identified in the embryos showing its relevancy as a model in ecotoxicogenomics. The draft Adverse Outcome Pathway was improved. Previously was hypothesized that gene regulation mechanisms were activated to synthesize more Ca channel proteins e this was confirmed here. Further, novel evidences were that, besides the extracellular competition, Cd competes intracellularly which causes a reduction in Ca efflux, and potentiates Cd embryotoxicity.
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Project description:Cadmium (Cd) influence in rice is a growing global environmental concern. Although many miRNAs and target genes have been identified in rice exposure to Cd stress, no comprehensive study has been done comprising integrative analysis of small RNAs, degradome and transcriptome sequencing to identify Cd-regulated miRNAs and their targets under Cd stress. In this study, 40 miRNAs including 38 known miRNAs representing 22 miRNA families and 2 novel miRNAs were substantially altered in response to Cd exposure. 18 differentially altered target genes were inversely correlated with 18 Cd responsive miRNAs. Majority of these targeted genes are transcript factors such as Auxin response factor 13 (ARF13), Scarecrow-like protein 6 (SCL6), Squamosa promoter-binding-like proteins (SPLs), Nuclear transcription factor Y subunit A-6 (NFYA6), Gibberellin-dependent avian myeloblastosis virus oncogene (GAMYB) and No apical meristem protein domain containing proteins (NACs), most of which were involved in signal transduction such as abscisic acid (ABA), Auxin, Gibberellin acid (GA) and MAPK (Mitogen-activated protein kinase). Functional analysis revealed that genes involved in photosynthesis pathway (osa00196, osa00195 and osa00710) and protein degradation pathway (osa04612) were identified to be participated in response to Cd in rice, including osa-miR156I-5p_R-1/SPLs, osa-miR171a_1ss12CT/DEGP10 and osa-miR169r-5p_R/NFYA6 circuits, respectively. We conclude that a combination of transcriptome, sRNAs and the degradome would confer a useful approach to investigate miRNA-mediated molecular mechanisms underlying plant response to Cd stress.
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Project description:We hypothesised that gestational exposure to chlordecone (CD) can lead to alteration of epigenetic landscape, specifically marks associated with transcriptional activity of the genes, such as H3K4me3 marks. We performed ChIP using anti-H3K4me3 commercial antibody (Millipore - 07-473). DNA-protein complexes were immunoprecipitated, eluted and then DNA were purified. We prepared libraries using NEBNext Ultra II DNA Library Prep Kit for Illumina. 13 libraries were prepared: 6 control, 6 CD-exposed and 1 input. After pre-processing of the sequencing data, we performed a comparison of peaks occupancy between control and exposed samples.
2021-04-08 | GSE171285 | GEO
Project description:Cadmium is a neurotoxic compound which induces cognitive alterations similar to those produced by Alzheimer's disease (AD). Autophagic flux impairment is a hallmark in Cd-induced AD-like pathology. However, the underlying mechanism remains obscure. In these study, Neuro-2a cells were exposed to different concentrations of Cd (1, 2, and 4 μM) for 72 h, and C57 mice (8 week) were orally administered Cd for 12 weeks. Chronic Cd exposure inhibited autophagosome-lysosome fusion and impaired lysosomal function, thereby contributing to defects in autophagic clearance and subsequently leading to APP accumulation and nerve cell death. Mechanistically, proteomic analysis coupled with Ingenuity Pathway Analysis identified the crucial key target molecule in Cd-impaired autophagic flux. Four-dimensional label-free succinylation quantitative proteomics were performed in Neuro-2a cells with and without 4 μM CdCl2 treatment for 72h. Then, vital molecules and crucial succinylation sites were identified. Moreover, the function and important role of the resulting molecule with crucial succinylation site were determined. These results may thus open an avenue for therapeutic intervention in chronic Cd-induced AD-like pathology.
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