Ontology highlight
ABSTRACT:
PROVIDER: PRJEB47148 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR6558310_1.fastq.gz | Fastqsanger.gz | |||
| ERR6558310_2.fastq.gz | Fastqsanger.gz | |||
| ERR6558311_1.fastq.gz | Fastqsanger.gz | |||
| ERR6558311_2.fastq.gz | Fastqsanger.gz | |||
| ERR6558312_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Chlordecone (CLD) is a pesticide used to control the banana weevill in the French West Indies from 1970 to 1993. Despite its ban in the 90s, the highly persistence of CLD and contamination of the food webs raised tremendous concern for public health [1]. CLD can induce reprotoxic, neurotoxic and hepatotoxic effects in humans and is involved in prostate cancer [2] and liver fibrosis potentiation [3]. In liver, although CLD is metabolized into phase I metabolite chlordecol (CLD-OH), it is highly biopersistent. Nevertheless, the cellular hepatic effects of these 2 compounds have been poorly described. Therefore, we used an original approach to investigate in vitro toxicity responses of CLD and CLD-OH in liver cell models (HepaRG cells and primary human hepatocytes, PHHs) using metabolomics and proteomics. 1) Resiere, D., et al. (2023). Chlordecone (Kepone) poisoning in the French Territories in the Americas. Lancet 401, 916. 2) Multigner L., et al. (2010). Chlordecone exposure and risk of prostate cancer. J Clin Oncol 28, 3457-3462. 3) Tabet E., et al. (2016). Chlordecone potentiates hepatic fibrosis in chronic liver injury induced by carbon tetrachloride in mice. Toxicol Lett 255, 1-10.
2025-06-10 | PXD043763 | Pride
Project description:Chlordecone (CLD) is a pesticide used to control the banana weevill in the French West Indies from 1970 to 1993. Despite its ban in the 90s, the highly persistence of CLD and contamination of the food webs raised tremendous concern for public health [1]. CLD can induce reprotoxic, neurotoxic and hepatotoxic effects in humans and is involved in prostate cancer [2] and liver fibrosis potentiation [3]. In liver, although CLD is metabolized into phase I metabolite chlordecol (CLD-OH), it is highly biopersistent. Nevertheless, the cellular hepatic effects of these 2 compounds have been poorly described. Therefore, we used an original approach to investigate in vitro toxicity responses of CLD and CLD-OH in liver cell models (HepaRG cells and primary human hepatocytes, PHHs) using metabolomics and proteomics. 1) Resiere, D., et al. (2023). Chlordecone (Kepone) poisoning in the French Territories in the Americas. Lancet 401, 916. 2) Multigner L., et al. (2010). Chlordecone exposure and risk of prostate cancer. J Clin Oncol 28, 3457-3462. 3) Tabet E., et al. (2016). Chlordecone potentiates hepatic fibrosis in chronic liver injury induced by carbon tetrachloride in mice. Toxicol Lett 255, 1-10.
2025-06-10 | PXD043683 | Pride
Project description:The study investigated the ability of selected (hyper-)thermophilic prokaryotes to grow anaerobically by the reduction of perchlorate and chlorate. Physiological, genomic and proteome analyses suggest that the Crenarchaeon Aeropyrum pernix reduces (per)chlorate with a periplasmic enzyme related to nitrate reductases, while it lacks a functional chlorite-disproportionating enzyme (Cld). A. pernix seems to rely on the chemical reactivity of reduced sulfur compounds with the toxic intermediate chlorite to complete the pathway. The chemical oxidation of thiosulfate (in excessive amounts present in the medium) to sulfate and the concomitant release of chloride anions from the reduction of chlorite are the products of a biotic-abiotic (per)chlorate reduction pathway in A. pernix. The apparent absence of Cld in two other (per)chlorate-reducing microorganisms and their dependence on sulfide for (per)chlorate reduction is consistent with earlier-made observations on (per)chlorate-reducing Archaeoglobus fulgidus. All here discussed microorganisms use strategies for complete (per)chlorate reduction that differ from the physiology of classical (per)chlorate-reducing mesophiles.
2017-06-02 | PXD001683 | Pride
Project description:Microbial community of a chlordecone contaminated nitisol subject to a remediation process based on chemical reduction
| PRJEB9579 | ENA
Project description:Selective, efficient, and controllable oxidation of cytosine modifications is valuable for epigenetic analyses, yet only limited progress has been made. Here, we present two modular chemical oxidation reactions: conversion of 5-hydroxymethylcytosine (5hmC) into 5-formylcytosine (5fC) utilizing 4-acetamido-2,2,6,6-tetramethylpiperidine-1-oxoammonium tetrafluoroborate (ACT+ BF4–) and further transformation of 5fC into 5-carboxycytosine (5caC) through Pinnick oxidation. Both reactions are mild and efficient on double-stranded DNA. We integrated these two oxidations with borane reduction to develop chemical-assisted pyridine borane sequencing plus (CAPS+), for direct and quantitative mapping of 5hmC. Compared with chemical-assisted pyridine borane sequencing (CAPS), CAPS+ improved the conversion rate and false-positive rate. We applied CAPS+ to mouse embryonic stem cells (mESCs) DNA, human normal brain and glioblastoma DNA samples, and demonstrated its superior sensitivity in analyzing the hydroxymethylome
2023-03-15 | GSE214006 | GEO
Project description:Exposure to pesticide chlordecone is associated with high risk of prostate cancer.We hypothesised that changes in histone H3K4me3 could be involved in pathological processes in prostate induced by chlordecone. We exposed mice to chlordecone during embryonic development (E6.5-E15.5) and we analysed F1 progeny male epigenetic H3K4me3 marks in prostate tissue, as well as H3K4me3 in the prostate of F3 progeny to reveal the transgenerational effects resulting from the ancestral exposure to CD. We performed ChIP using H3K4me3 commercial antibody (Merck Millipore, 07-473) and pooled prostate tissues from 4 mice. DNA-protein complex was immunoprecipitated, eluted and DNA purified.
2021-04-01 | GSE135199 | GEO
Project description:Background/Aims: Cholestatic liver diseases (CLD) are the leading indication for pediatric liver transplantation. Increased intrahepatic bile acid concentrations cause endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) is activated to maintain homeostasis. UPR dysregulation, including the inositol-requiring enzyme 1α/X-box protein 1 (IRE1α/XBP1) pathway, is associated with several adult liver diseases. We evaluated hepatic UPR expression in pediatric patients with end-stage CLD and hypothesize that an inability to appropriately activate the hepatic IRE1α/XBP1 pathway is associated with the pathogenesis of CLD. Methods: We evaluated 34 human liver explants. Cohorts included: pediatric CLD (Alagille, ALGS, and progressive familial intrahepatic cholestasis, PFIC), pediatric non-cholestatic liver disease controls (autoimmune hepatitis, AIH), adult CLD, and normal controls. We performed RNA-seq, quantitative PCR, and western blotting to measure expression differences of the hepatic UPR and other signaling pathways. Results: Metascape pathway analysis demonstrated that the KEGG ‘protein processing in ER’ pathway was downregulated in pediatric CLD compared to normal controls. Pediatric CLD had decreased hepatic IRE1α/XBP1 pathway gene expression and decreased protein expression of p-IRE1α compared to normal controls. These CLD changes were not disease-specific to ALGS or PFIC. IRE1α/XBP1 pathway gene expression was decreased in pediatric CLD compared to AIH disease controls. Conclusion: Pediatric CLD explants have decreased gene and protein expression of the protective IRE1α/XBP1 pathway and down-regulated KEGG protein processing in the ER pathways. IRE1α/XBP1 pathway expression differences occur when compared to both normal and non-cholestatic disease controls. Attenuated expression of the IRE1α/XBP1 pathway is associated with cholestatic diseases and could be targeted to treat pediatric CLD.
2022-06-23 | GSE206364 | GEO
Project description:We hypothesized that gestational exposure to chlordecone can lead to alteration of murine ovary's epigenetic landscape. To test our hypothesis, we exposed mice to chlordecone during embryonic development and we analyzed F1 female progeny epigenetic mark H3K4me3 in ovaries. We performed ChIP using anti-H3K4me3 commercial antibody (Merck Millipore, 07-473). DNA-protein complexes were immunoprecipitated, eluted and then DNA were purified.
2019-05-21 | GSE129897 | GEO
Project description:Patients with chronic liver disease (CLD), including cirrhosis, are at increased risk of intractable viral infections and are hyporesponsive to vaccination. Hallmarks of CLD and cirrhosis include microbial translocation and elevated levels of type I interferon (IFN-I). We aimed to investigate the relevance of microbiota-induced IFN-I in the impaired adaptive immune responses observed in CLD. We combined bile duct ligation (BDL) and carbon tetrachloride (CCl4) models of liver injury with vaccination or lymphocytic choriomeningitis virus infection in transgenic mice lacking IFN-I in myeloid cells (LysM-Cre IFNARflox/flox), IFNAR-induced IL-10 (MX1-Cre IL10flox/flox) or IL-10R in T cells (CD4-DN IL-10R). Key pathways were blocked in vivo with specific antibodies (anti-IFNAR and anti-IL10R). We assessed T-cell responses and antibody titers after HBV and SARS-CoV-2 vaccinations in patients with CLD and healthy individuals in a proof-of-concept clinical study. We demonstrate that BDL- and CCL4-induced prolonged liver injury leads to impaired T-cell responses to vaccination and viral infection in mice, subsequently leading to persistent infection. We observed a similarly defective T-cell response to vaccination in patients with cirrhosis. Innate sensing of translocated gut microbiota induced IFN-I signaling in hepatic myeloid cells that triggered excessive IL-10 production upon viral infection. IL-10R signaling in antigen-specific T cells rendered them dysfunctional. Antibiotic treatment and inhibition of IFNAR or IL-10Ra restored antiviral immunity without detectable immune pathology in mice. Notably, IL-10Ra blockade restored the functional phenotype of T cells from vaccinated patients with cirrhosis. Innate sensing of translocated microbiota induces IFN-/IL-10 expression, which drives the loss of systemic T-cell immunity during prolonged liver injury.
2023-09-11 | GSE158261 | GEO