Transcriptomics of Nickel and Cobalt toxicity in Paramecium
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PROVIDER: PRJEB61118 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional profiling of the digestive gland tissue of female mussel Mytilus galloprovincialis exposed to nickel along with a temperature gradient Background: The exposure of marine organisms to stressing agents may affect the level and pattern of gene expression. Although many studies have examined the ecological effects of heat stress on mussels, little is known about the physiological mechanisms that might be affected by co-exposure to heat stress and environmental contaminants such as nickel (Ni). In the present work we investigated the effects of simultaneous changes in temperature and Ni supply on lysosomal membrane stability (LMS) and malondialdehyde accumulation (MDA) in the digestive gland (DG) of the blue mussel Mytilus galloprovincialis (Lam.). To shed some light into how the molecular response to environmental stressors is modulated, we employed a cDNA microarray with 1,673 sequences to measure the relative transcript abundances in the DG of mussels exposed to Ni along with the temperature increase. Temperature and Ni rendered additive effects on LMS and MDA accumulation, increasing the toxic effects of metal cations. Ni loads in DG tissues was also affected by co-exposure to 26°C. In animals exposed only to heat stress, functional genomics analysis of the microarray data (171 DEGs) revealed 7 biological processes, largely dominated by the up-regulation of folding protein-related genes, and the down regulation of genes involved in cell migration and cellular component assembly. Exposure to Ni at 18°C and 26°C rendered respectively 188 and 262 DEGs showing distinct pattern in term of biological processes. In particular, the response of mussels exposed to Ni at 26°C was characterized by the up regulation of proteolysis, ribosome biogenesis, response to unfolded proteins and catabolic-related genes as well as the down-regulation of genes encoding cellular metabolic processes. Our data provide new insights on the transcriptomic response in mussels challenging temperature increases and Ni exposure and should be carefully considered in view of the biological effects of heat stress and particularly in polluted areas.
2013-06-19 | GSE48062 | GEO
Project description:The effect of nanomaterials (NMs) is less understood in light of the implemented and existing methodologies for regular chemicals. To understand the mode of action of NMs is one of the alternatives to improve predictions and environmental risk assessment (ERA). In the present work the high-throughput gene expression tool (4x44K microarray for Enchytraeus crypticus) was used to investigate the mechanisms activated by Ni exposure. Ni nanoparticles (Ni-NPs) were investigated together with Ni-salt (NiNO3). Testing was done based on reproduction effect concentrations (EC20, EC50) using 3 and 7 days exposure periods.
2017-06-13 | GSE69793 | GEO
Project description:Cobalt (Co) and Nickel (Ni) are used nowadays in various industrial applications like lithium-ion batteries, raising concerns about their environmental release and public health threats. Both metals are potentially carcinogenic and may cause neurological and cardiovascular dysfunctions, though underlying toxicity mechanisms have to be further elucidated. This study employs untargeted transcriptomics to analyze downstream cellular effects of individual and combined Co and Ni toxicity in human liver carcinoma cells (HepG2). The results reveal a synergistic effect of Co and Ni, leading to significantly higher number of differentially expressed genes (DEGs) compared to individual exposure. There was a clear enrichment of Nrf2 regulated genes linked to pathways such as glycolysis, iron and glutathione metabolism, and sphingolipid metabolism, confirmed by targeted analysis. Co and Ni exposure alone and combined caused nuclear Nrf2 translocation, while only combined exposure significantly affects iron and glutathione metabolism, evidenced by upregulation of HMOX-1 and iron storage protein FTL. Both metals impact sphingolipid metabolism, increasing dihydroceramide levels and decreasing ceramides, sphingosine and lactosylceramides, along with diacylglycerol accumulation. By combining transcriptomics and analytical methods, this study provides valuable insights into molecular mechanisms of Co and Ni toxicity, paving the way for further understanding of metal stress.
| S-EPMC11345407 | biostudies-literature
Project description:Transcriptional profiling of the digestive gland tissue of female mussel Mytilus galloprovincialis exposed to nickel along with a temperature gradient Background: The exposure of marine organisms to stressing agents may affect the level and pattern of gene expression. Although many studies have examined the ecological effects of heat stress on mussels, little is known about the physiological mechanisms that might be affected by co-exposure to heat stress and environmental contaminants such as nickel (Ni). In the present work we investigated the effects of simultaneous changes in temperature and Ni supply on lysosomal membrane stability (LMS) and malondialdehyde accumulation (MDA) in the digestive gland (DG) of the blue mussel Mytilus galloprovincialis (Lam.). To shed some light into how the molecular response to environmental stressors is modulated, we employed a cDNA microarray with 1,673 sequences to measure the relative transcript abundances in the DG of mussels exposed to Ni along with the temperature increase. Temperature and Ni rendered additive effects on LMS and MDA accumulation, increasing the toxic effects of metal cations. Ni loads in DG tissues was also affected by co-exposure to 26M-BM-0C. In animals exposed only to heat stress, functional genomics analysis of the microarray data (171 DEGs) revealed 7 biological processes, largely dominated by the up-regulation of folding protein-related genes, and the down regulation of genes involved in cell migration and cellular component assembly. Exposure to Ni at 18M-BM-0C and 26M-BM-0C rendered respectively 188 and 262 DEGs showing distinct pattern in term of biological processes. In particular, the response of mussels exposed to Ni at 26M-BM-0C was characterized by the up regulation of proteolysis, ribosome biogenesis, response to unfolded proteins and catabolic-related genes as well as the down-regulation of genes encoding cellular metabolic processes. Our data provide new insights on the transcriptomic response in mussels challenging temperature increases and Ni exposure and should be carefully considered in view of the biological effects of heat stress and particularly in polluted areas. Digestive gland tissue from individual animals in different experimental conditions were analyzed in a complete loop design. Dual color competitive hybridizations (Control M-bM-^@M-^\16M-BM-0CM-bM-^@M-^] vs M-bM-^@M-^\20M-BM-0CM-bM-^@M-^] vs M-bM-^@M-^\24M-BM-0CM-bM-^@M-^] vs M-bM-^@M-^\16M-BM-0C+CuM-bM-^@M-^], M-bM-^@M-^\20M-BM-0CM-bM-^@M-^] vs M-bM-^@M-^\24M-BM-0CM-bM-^@M-^] vs M-bM-^@M-^\20M-BM-0C+CuM-bM-^@M-^], M-bM-^@M-^\24M-BM-0CM-bM-^@M-^] vs M-bM-^@M-^\24M-BM-0C+CuM-bM-^@M-^], M-bM-^@M-^\16M-BM-0C+CuM-bM-^@M-^] vsM-bM-^@M-^]20M-BM-0C+CuM-bM-^@M-^] vs M-bM-^@M-^\24M-BM-0C+CuM-bM-^@M-^]; M-bM-^@M-^\20M-BM-0C+CuM-bM-^@M-^] vs M-bM-^@M-^\24M-BM-0C+CuM-bM-^@M-^]) including label swap. Single individuals. Four biological replicates. One replicate per array.
2013-06-19 | E-GEOD-48062 | biostudies-arrayexpress
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
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 | GSE139355 | GEO
Project description:To study the mechanisms of Ni resistance in the metal resistant Acidiphilium sp. PM, the transcriptome of Acidiphilium sp. PM was studied 5min and 30 min after the addition of 10mM Ni and compared to the transcriptome in untreated cells.
2013-06-18 | GSE48042 | GEO
Project description:Purpose: Environmentally induced diseases, including cancer typically develop long after the exposure has occurred. However, most of the toxicological studies are conducted during active exposure. Therefore, environmental exposure-induced adverse effects that persist after cessation of exposure is poorly understood. Methods: Immortalized human bronchial epithelial cells (BEAS-2B) were cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Cellgro) supplemented with 1% Penicillin Streptomycin and 10% Fetal Bovine Serum (FBS, Atlanta Biologicals) at 37 degree C and 5 % CO2. For Ni exposure, various concentrations of NiCl2 (Sigma N6136) was added to the media and the cells were cultured for 6 weeks. Following exposure, the cells were washed and cultured in Ni-free medium for 2 weeks to obtain the Ni-washed-out cells. To obtain homogenous populations of Ni-exposed cells, the cells exposed to 100 mM NiCl2 for 6 weeks were plated in 15 cm plates in Ni-free medium at the rate of 1000, 500, 100 and 50 cells per plate. Nicely separated single colonies were picked and the populations were expanded in Ni-free medium. Results: Here we report that Ni, an environmentally prevalent, low-mutagenic carcinogen causes epithelial-mesenchymal transition (EMT) that persists even after the exposure has ceased. Ni-induced persistent EMT induction is dependent on the upregulation of ZEB1, an EMT master regulator. We found that Ni exposure resolved the bivalent chromatin environment of ZEB1 gene, thereby keeping it in a permanent ‘on’ state. The continuously expressing ZEB1 downregulated its negative regulators, thus establishing a self-sustaining positive regulatory loop. Given the importance of EMT in a number of diseases including asthma, pulmonary fibrosis, development of premalignancy, carcinogenesis and metastasis, we believe that persistent EMT induction through epigenetic activation of ZEB1 is a major step in Ni-induced human diseases.
2018-03-17 | GSE95180 | GEO
Project description:Ni and Co are individually and combined treated to HepG2 cells
| PRJEB76248 | ENA
Project description:To study the mechanisms of Ni resistance in the metal resistant Acidiphilium sp. PM, the transcriptome of Acidiphilium sp. PM was studied 5min and 30 min after the addition of 10mM Ni and compared to the transcriptome in untreated cells. Two-condition hybridization experiments: untreated cells vs cells treated with 10mM Ni (for either 5 or 30 minutes). Eighteen 100ml-cultures: 6 untreated control cultures (not exposed to Ni), 6 cultures exposed to 10mM Ni for 5min, and 6 cultures exposed to 10mM Ni for 30 min. Cultures were independently grown and harvested. Gene expression levels of one untreated replicate were compared separately with one 5min-exposed replicate and with one 30min-exposed replicate (yielding two microarray data sets. One for each hybridization).
2013-06-18 | E-GEOD-48042 | biostudies-arrayexpress