Expression data from L3 stage Caernorhabditis elegans after arsenic exposure
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ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE39012 | GEO | 2012/06/29
SECONDARY ACCESSION(S): PRJNA169608
REPOSITORIES: GEO
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Project description:We used microarrays to explore the global affect on gene expression in C. elegans after exposure to arsenic L3 stage N2 worms were incubated for 6 hrs in sodium arsenite containing media of concentrations .003 and .03. Three independent extractions of RNA were performed from no exposure, .003 exposure, and .03 exposure worms.
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Project description:To identified the differential expressed genes between the arsenic exposure cells and wild type cells As is a well- known carcinogen, it receives special attention. Due to its ubiquitous distribution in the environment, a unicellular model system related to the environment will be useful in toxicological research of arsenic. The eukaryotic protist Tetrahymena thermophila is a well-established model in classical toxicology and now a potential model at genomic level. In the present study, Tetrahymena thermophila was inbred with arsenate. With the use of microarray technique, the genes differentially expressed at 4 time points in exposure to arsenate were screened out. The major biological processes involved and their changes over time were identified with enrichment analysis and transformed expression data. Characteristics of arsenic toxicity and response to arsenic were identified, proving T. thermophila a good unicellular model for arsenic toxicological research at genomic level.
2019-12-01 | GSE53836 | GEO
Project description:Arsenic and mercury are known chemical hazards. The differences in effects from organic and inorganic forms of these toxic elements is less well understood, however. The nematode Caenorhabditis elegans (C. elegans) is a suitable model to investigate the toxicity of environmental hazards. In this study, the transcriptomic profiles of C. elegans exposed to inorganic mercury chloride (HgCl2) and sodium (meta)arsenite (NaAsO2) were assessed alongside organic methylmercury chloride (meHgCl) and dimethylarsinic acid (DMA). For this purpose, adult C. elegans were exposed for 24 h to NaAsO2 (10 µg/ml), DMA (200 µg/ml), HgCl2 (2 µg/ml), and meHgCl (0.5 µg/ml), concentrations that were equitoxic in juveniles for developmental delay. Whole genome gene expression profiles were determined by using Cellegans_UnrestrictedGE_G2519F_020186 Microarray (Agilent Technologies, Santa Clara, CA). The results showed significant changes in the transcriptome of adult C. elegans exposed to NaAsO2, DMA, HgCl2, or meHgCl relative to the control group (C. elegans treated with water). A total of 927 and 1221 differentially expressed genes (DEGs) were found in C. elegans treated with 10 µg/ml NaAsO2 or 200 µg/ml DMA, respectively. Interestingly, only 161 DEGs were in common for these two chemicals. Exposure to 2 µg/ml HgCl2 or 0.5 µg/ml meHgCl altered the expression of 670 and 485 genes, respectively, and out of these genes, 154 were commonly altered by the two treatments. Analysis of DEGs revealed that organic and inorganic forms of arsenic and mercury have different effects on the transcriptome of adult C. elegans.
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Project description:Chronic exposure to arsenic is associated with dermatological and non-dermatological disorders. Consumption of arsenic contaminated drinking water results in accumulation of arsenic in liver, spleen, kidneys, lungs and gastrointestinal tract. Although, arsenic is cleared from these sites, a substantial amount of residual arsenic is left in keratin-rich tissues such as skin. Epidemiological studies on arsenic suggest the association of skin cancer upon arsenic exposure, however, the exact mechanism of arsenic induced carcinogenesis is not completely understood. We have developed a cell line-based model to understand the molecular mechanisms involved in arsenic mediated toxicity and carcinogenicity. Human skin keratinocyte cell line, HaCaT was exposed to 100nM sodium arsenite for six months. We observed an increase in the basal ROS levels in arsenic exposed cells along with the increase in anti-apoptotic proteins. SILAC-based quantitative proteomics approach resulted in the identification and quantitation of 2,181 proteins of which 39 proteins were found to be overexpressed (≥2-fold) and 56 downregulated (≤2-fold) upon chronic arsenic exposure. Our study provides comprehensive insights into the molecular basis of chronic arsenic exposure on skin.
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Project description:The Biomarkers of Exposure to ARsenic (BEAR) pregnancy cohort in Gómez Palacio, Mexico was recently established to better understand the impacts of prenatal exposure to inorganic arsenic (iAs). In this study, we examined a subset (n = 40) of newborn cord blood samples for microRNA (miRNA) expression changes associated with in utero arsenic exposure. Levels of iAs in maternal drinking water (DW-iAs) and maternal urine were assessed. Levels of DW-iAs ranged from below detectable values to 236 µg/L (mean = 51.7 µg/L). Total arsenic in maternal urine (U-tAs) was defined as the sum of iAs and its monomethylated and dimethylated metabolites (MMAs and DMAs, respectively) and ranged from 6.2 to 319.7 µg/L (mean = 64.5 µg/L). Genome-wide miRNA expression analysis of cord blood revealed 12 miRNAs with increasing expression associated with U-tAs. Transcriptional targets of the miRNAs were computationally predicted and subsequently assessed using transcriptional profiling. Pathway analysis demonstrated that the U-tAs-associated miRNAs are involved in signaling pathways related to known health outcomes of iAs exposure including cancer and diabetes mellitus. Immune response-related mRNAs were also identified with decreased expression levels associated with U-tAs, and predicted to be mediated in part by the arsenic-responsive miRNAs. Results of this study highlight miRNAs as novel responders to prenatal arsenic exposure that may contribute to associated immune response perturbations.
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Project description:The Biomarkers of Exposure to ARsenic (BEAR) pregnancy cohort in Gómez Palacio, Mexico was recently established to better understand the impacts of prenatal exposure to inorganic arsenic (iAs). In this study, we examined a subset (n = 40) of newborn cord blood samples for microRNA (miRNA) expression changes associated with in utero arsenic exposure. Levels of iAs in maternal drinking water (DW-iAs) and maternal urine were assessed. Levels of DW-iAs ranged from below detectable values to 236 µg/L (mean = 51.7 µg/L). Total arsenic in maternal urine (U-tAs) was defined as the sum of iAs and its monomethylated and dimethylated metabolites (MMAs and DMAs, respectively) and ranged from 6.2 to 319.7 µg/L (mean = 64.5 µg/L). Genome-wide miRNA expression analysis of cord blood revealed 12 miRNAs with increasing expression associated with U-tAs. Transcriptional targets of the miRNAs were computationally predicted and subsequently assessed using transcriptional profiling. Pathway analysis demonstrated that the U-tAs-associated miRNAs are involved in signaling pathways related to known health outcomes of iAs exposure including cancer and diabetes mellitus. Immune response-related mRNAs were also identified with decreased expression levels associated with U-tAs, and predicted to be mediated in part by the arsenic-responsive miRNAs. Results of this study highlight miRNAs as novel responders to prenatal arsenic exposure that may contribute to associated immune response perturbations.
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Project description:Arsenic exposure is considered as a risk factor for lung cancer. However, toxic effects of the metabolic mechanism responsible for arsenic-induced toxicity and especially chronic effects, are less known. Here we constructed a cell model of lung adenocarcinoma A549 cells by chronic arsenic exposure. Cell-based experiments showed that A549 cells display platinum resistance with chronic exposure of arsenic. The metabolic response of A549 cells to arsenic exposure was profiled by gas chromatography-mass spectrometry.
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Project description:In the present study, we employed the RNA sequencing platform to examine the molecular response of zebrafish liver to arsenic exposure and carry out detailed transcriptomic analyses for further understanding of molecular toxicity. We found that several important biological processes were perturbed by arsenic exposure, including oxidation reduction, translation, iron ion transport, cell redox and homeostasis, as well as related pathways in metabolism and diseases. Furthermore, as there are currently no biomarker genes available for predicting arsenic exposure, we took the advantage of RNA sequencing platform to identify most suitable biomarker genes from top responsive genes to arsenic exposure. We first validated these top responsive genes by RT-qPCR in zebrafish and then in Japanese medaka (Oryzias latipes) at individual fish level for more robustly responsive genes across different fish species.
2013-09-04 | GSE48427 | GEO
Project description:Modulation of signaling pathways upon chronic arsenic exposure remains poorly studied. Here we carried out SILAC-based quantitative phosphoproteomics analysis to dissect the signaling induced upon chronic arsenic exposure in human skin keratinocyte cell line, HaCaT. We identified 4,171 unique phosphosites derived from 2,000 proteins. We observed differential phosphorylation of 406 phosphosites (2-fold) corresponding to 305 proteins. Several pathways involved in cytoskeleton maintenance and organization were found to be significantly enriched (p<0.05). Our data revealed altered phosphorylation of proteins associated with adherens junction remodeling and actin polymerization. Kinases such as protein kinase C iota type (PRKCI), mitogen-activated protein kinase kinase kinase 1 (MAP3K1), tyrosine-protein kinase BAZ1B (BAZ1B) and STE20 like kinase (SLK) were found to be hyperphosphorylated. Our study provides novel insights into signaling perturbations associated with chronic arsenic exposure in human skin keratinocytes.
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