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PROVIDER: PRJNA170663 | ENA |
REPOSITORIES: ENA
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Project description:Nanotoxicogenomic study of ZnO and TiO2 responses (Illumina)
| PRJNA170661 | ENA
Project description:This study evaluated transcriptional effects of particles smaller than 100 nm of TiO2 and ZnO. Based on previous data in colon cancer cells (GSE14910), we evaluated HaCaT and Sk Mel-28 cells for transcriptional responses to 1 and 5 ug/cm2 ZnO, or 5 and 10 ug/cm2 TiO2. No particle controls were also included. Again, the most pronounced transcriptional response resulted from ZnO treatement with little responses to TiO2. We identified increased protein stress responses, decreased regulation of transcription, and responses to Zn ions. We did not observe the protein stress response and regulation of transcription with soluble Zn. Keywords: skin-derived cancer cells - response to ZnO nanoparticulate
2011-11-01 | GSE25167 | GEO
Project description:This study evaluated transcriptional effects of particles smaller than 100 nm of TiO2 and ZnO. Based on previous data in colon cancer cells (GSE14910), we evaluated HaCaT and Sk Mel-28 cells for transcriptional responses to 1 and 5 ug/cm2 ZnO, or 5 and 10 ug/cm2 TiO2. No particle controls were also included. Again, the most pronounced transcriptional response resulted from ZnO treatement with little responses to TiO2. We identified increased protein stress responses, decreased regulation of transcription, and responses to Zn ions. We did not observe the protein stress response and regulation of transcription with soluble Zn. Keywords: skin-derived cancer cells - response to ZnO nanoparticulate Two skin-derived cancer cell types (HaCaT and SK Mel-28) were treated with media containing the nanoparticulate, ZnCl2, or ZnO separated from the HaCaTs by a Transwell insert, and RNA was collected after 4 hrs. Generally, the RNA from 4 independent samples were combined for one microarray.
2011-11-01 | E-GEOD-25167 | biostudies-arrayexpress
Project description:ZnO and TiO2 nanoparticles can elicit a range of perturbed cell responses in vitro. Exposure to topically applied sunscreens containing ZnO or TiO2 particles may or may not elicit a biological effect in mice. We aimed to compare the biological responses of immune-competent hairless mice receiving topical applications of commercially available sunscreens with or without metal oxide nanoparticles, with the responses of mice receiving no sunscreen.
2016-07-26 | GSE84818 | GEO
Project description:ZnO and TiO2 nanoparticles can elicit a range of perturbed cell responses in vitro. Exposure to topically applied sunscreens containing ZnO or TiO2 particles may or may not elicit a biological effect in mice. We aimed to compare the biological responses of immune-competent hairless mice receiving topical applications of commercially available sunscreens with or without metal oxide nanoparticles, with the responses of mice receiving no sunscreen. Commercially available sunscreens containing ZnO nanoparticles, a mixture of TiO2 nanoparticles and organic UVR filters, or only organic UVR filters were applied to the backs of SKH:QS mice weekly over 36 weeks, with or without subsequent exposure to 29 kJ/m2 UVR. After 36 weeks and 30 treatments, mice were sacrificed and liver tissue was harvested for RNA isolation and whole genome transcriptional profiling, comparing the expression profiles of treated mice with untreated mice.
2016-07-26 | E-GEOD-84818 | biostudies-arrayexpress
Project description:A comprehensive in vitro assessment of two commercial metal oxide nanoparticles, TiO2 and ZnO, was performed using human monocyte-derived macrophages (HMDM), monocyte-derived dendritic cells (MDDC), and T cell leukemia-derived cell line (Jurkat). TiO2 nanoparticles were found to be non-toxic whereas ZnO nanoparticles caused dose-dependent cell death. Subsequently, global gene expression profiling was performed to identify signaling pathways underlying the cytotoxicity caused by ZnO nanoparticles. Analysis was done with doses, 1M-BM-5g/ml and 10M-BM-5g/ml after 6 and 24 hours of exposure. Interestingly, 2703 genes were significantly differentially expressed in HMDM upon exposure to 10M-BM-5g/ml ZnO nanoparticles, while in MDDCs only 12 genes were affected. In Jurkat cells, 980 genes were differentially expressed. It is noteworthy that the gene expression of metallothioneins was upregulated in all the three cell types. In addition to the common ZnO-inducible changes, a notable proportion of the genes were regulated in a cell type-specific manner. Using a panel of ZnO nanoparticles, we obtained an additional support that the cellular response to ZnO nanoparticles is caused by particle dissolution. Gene ontology analysis revealed that the top biological processes disturbed in HMDM and Jurkat cells were regulating cell death and growth. In addition, genes controlling immune system development were affected. Bioinformatics assessment showed that the top human disease category associated with ZnO-responsive genes in both HMDM and Jurkat cells was cancer. Overall, the study revealed novel genes and pathways for mediating ZnO nanoparticle-induced toxicity and demonstrated the value of assessing nanoparticle responses through combined transcriptomics and bioinformatics approach. Altogether 90 samples were analyzed originating from three biological replicates of HMDM, MDDC or Jurkat cells containg untreated control cells, ZnO or TiO2 treated cells with doses 1M-BM-5g/ml and 10M-BM-5g/ml. The sample timepoints were 6 hours and 24 hours.
2013-07-25 | E-GEOD-39316 | biostudies-arrayexpress
Project description:A comprehensive in vitro assessment of two commercial metal oxide nanoparticles, TiO2 and ZnO, was performed using human monocyte-derived macrophages (HMDM), monocyte-derived dendritic cells (MDDC), and T cell leukemia-derived cell line (Jurkat). TiO2 nanoparticles were found to be non-toxic whereas ZnO nanoparticles caused dose-dependent cell death. Subsequently, global gene expression profiling was performed to identify signaling pathways underlying the cytotoxicity caused by ZnO nanoparticles. Analysis was done with doses, 1ug/ml and 10ug/ml after 6 and 24 hours of exposure. Interestingly, 2703 genes were significantly differentially expressed in HMDM upon exposure to 10ug/ml ZnO nanoparticles, while in MDDCs only 12 genes were affected. In Jurkat cells, 980 genes were differentially expressed. It is noteworthy that the gene expression of metallothioneins was upregulated in all the three cell types. In addition to the common ZnO-inducible changes, a notable proportion of the genes were regulated in a cell type-specific manner. Using a panel of ZnO nanoparticles, we obtained an additional support that the cellular response to ZnO nanoparticles is caused by particle dissolution. Gene ontology analysis revealed that the top biological processes disturbed in HMDM and Jurkat cells were regulating cell death and growth. In addition, genes controlling immune system development were affected. Bioinformatics assessment showed that the top human disease category associated with ZnO-responsive genes in both HMDM and Jurkat cells was cancer. Overall, the study revealed novel genes and pathways for mediating ZnO nanoparticle-induced toxicity and demonstrated the value of assessing nanoparticle responses through combined transcriptomics and bioinformatics approach. Nanoparticles used in the study: ZnO-1 commercial (IBU-tec advanced materials AG), ZnO-2 (mandelic acid coated ZnO-1), ZnO-3 (mercaptopropyl-trimethoxysilane coated ZnO-1), ZnO-4 (methoxyl coated ZnO), ZnO-5 (diethylene glycol modified ZnO) and ZnO-9 (folic acid modified ZnO). Detailed particle production and characterization data can be found from the articles: Buerki-Thurnherr et al. 2012 Nanotoxicology and Tuomela et al.
2013-07-25 | GSE39330 | GEO
Project description:This study evaluated transcriptional effects of particles smaller than 100 nm of carbon black, SiO2, Al2O3, TiO2, ZnO and Fe203. Since there is concern that inflammation may increase the uptake and/or toxicity of ultrafine particles, we evaluated the transcriptional responses without or with a TNFα pretreatment to mimic an inflammatory state. The most pronounced transcriptional response resulted from ZnO treatement, another response was to TNFα pre-treatment. We identified stress responses, responses to Zn ions, but did not observe a consistent proinflammatory response as evaluated by Gene Ontology of the genes that altered expression most as identified by significance analysis. Keywords: colon cancer cells - response to distinct nanoparticulate
2010-12-01 | GSE14910 | GEO
Project description:A comprehensive in vitro assessment of two commercial metal oxide nanoparticles, TiO2 and ZnO, was performed using human monocyte-derived macrophages (HMDM), monocyte-derived dendritic cells (MDDC), and T cell leukemia-derived cell line (Jurkat). TiO2 nanoparticles were found to be non-toxic whereas ZnO nanoparticles caused dose-dependent cell death. Subsequently, global gene expression profiling was performed to identify signaling pathways underlying the cytotoxicity caused by ZnO nanoparticles. Analysis was done with doses, 1µg/ml and 10µg/ml after 6 and 24 hours of exposure. Interestingly, 2703 genes were significantly differentially expressed in HMDM upon exposure to 10µg/ml ZnO nanoparticles, while in MDDCs only 12 genes were affected. In Jurkat cells, 980 genes were differentially expressed. It is noteworthy that the gene expression of metallothioneins was upregulated in all the three cell types. In addition to the common ZnO-inducible changes, a notable proportion of the genes were regulated in a cell type-specific manner. Using a panel of ZnO nanoparticles, we obtained an additional support that the cellular response to ZnO nanoparticles is caused by particle dissolution. Gene ontology analysis revealed that the top biological processes disturbed in HMDM and Jurkat cells were regulating cell death and growth. In addition, genes controlling immune system development were affected. Bioinformatics assessment showed that the top human disease category associated with ZnO-responsive genes in both HMDM and Jurkat cells was cancer. Overall, the study revealed novel genes and pathways for mediating ZnO nanoparticle-induced toxicity and demonstrated the value of assessing nanoparticle responses through combined transcriptomics and bioinformatics approach.
2013-07-25 | GSE39316 | GEO