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ABSTRACT:
PROVIDER: PRJNA1312041 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of Human bone mesenchymal stem cells treated separately with DMSO vehicle, 100 nM perfluorooctanesulfonat(PFOS), 100 nM perfluorooctanoic acid(PFOA), 100 nM perfluorohexanesulphonate(PFHxS) or100 nM Chlorinated polyfluoroalkyl ether sulfonate(F-53B) for 7 days. Results provide insight into the molecular mechanisms by which PFASs interfere with osteogenic differentiation potential in HBMSCs.
2019-12-31 | GSE115836 | GEO
Project description:These experiments have systematically assessed the potential utility of transcriptomic endpoints as enhancements to the guaiacol assay. Previously, we demonstrated that benzophenone-2, benzophenone, perfluorooctane sulfonate, bisphenol A bis ether, and vinclozolin decreased TPO activity, and that dibutyl phthalate, carbaryl, dibenzo(a,h)anthracene, benzo(a)pyrene, and methylmercury increased TPO activity. In this study, we used human oligonucleotide chips to examine changes in the gene expression profile of FTC-238 human follicular thyroid carcinoma cells expressing human recombinant TPO, after exposure of the cells to TPO activity-disrupting agents.
2011-11-09 | GSE30961 | GEO
Project description:The perfluorinated alkyl substance PFESA-BP2 (1,1,2,2-tetrafluoro-2-[1,1,1,2,3,3-hexafluoro-3-(1,1,2,2-tetrafluoroethoxy)propan-2-yl]oxyethane-1-sulfonic acid; also known as nafion BP2) has been detected in the blood of people living in the North Carolina Cape Fear River basin downstream of an industrial manufacturing facility. Given that almost nothing is known about the potential toxicity of PFESA-BP2 and safe exposure levels have not yet been determined, we performed a benchmark dose analysis of phenotypic and genomic effects. Female mice were exposed to PFESA-BP2 at 0, 0.03, 0.3, 3, and 6 mg/kg-day each day for 7 days by oral gavage. Transcript profiling showed that PFESA-BP2 activates a number of transcription factors linked to liver toxicity including constitutive activated/androstane receptor, pregnane X receptor, and Nrf2, but unlike other long-chain PFAS, there was only weak activation of peroxisome proliferator-activated receptor α. Steatosis was coincident with activation of sterol response element binding proteins as well as increases in the expression of the very low density lipoprotein receptor.
2022-12-01 | GSE147332 | GEO
Project description:The perfluorinated alkyl substance PFESA-BP2 (1,1,2,2-tetrafluoro-2-[1,1,1,2,3,3-hexafluoro-3-(1,1,2,2-tetrafluoroethoxy)propan-2-yl]oxyethane-1-sulfonic acid; also known as nafion BP2) has been detected in the blood of people living in the North Carolina Cape Fear River basin downstream of an industrial manufacturing facility. Given that almost nothing is known about the potential toxicity of PFESA-BP2 and safe exposure levels have not yet been determined, we performed a benchmark dose analysis of phenotypic and genomic effects. Male mice were exposed to PFESA-BP2 at 0, 0.03, 0.3, 3, and 6 mg/kg-day each day for 7 days by oral gavage. Transcript profiling showed that PFESA-BP2 activates a number of transcription factors linked to liver toxicity including constitutive activated/androstane receptor, pregnane X receptor, and Nrf2, but unlike other long-chain PFAS, there was only weak activation of peroxisome proliferator-activated receptor α. Steatosis was coincident with activation of sterol response element binding proteins as well as increases in the expression of the very low density lipoprotein receptor.
2022-12-01 | GSE147331 | GEO
Project description:Social anxiety disorder (SAD) is a psychiatric disorder characterized by severe fear in social situations and avoidance of these. Multiple genetic as well as environmental factors contribute to the etiopathology of SAD. One of the main risk factors for SAD is stress, especially during early periods of life (early life adversity; ELA). ELA leads to structural and regulatory alterations contributing to disease vulnerability. This includes the dysregulation of the immune response. However, the molecular link between ELA and the risk for SAD in adulthood remain largely unclear. Evidence is emerging that long-lasting changes of gene expression patterns play an important role in the biological mechanisms linking ELA and SAD. Therefore, we conducted a transcriptome study of SAD and ELA performing RNA sequencing in peripheral blood samples. Analyzing differential gene expression between individuals suffering from SAD with high or low levels of ELA and healthy individuals with high or low levels of ELA, 13 significantly differentially expressed genes (DEGs) were identified with respect to SAD whilst no significant differences in expression were identified with respect to ELA. The most significantly expressed gene was MAPK3 (p=0.003) being upregulated in the SAD group compared to control individuals. In contrary, weighted gene co-expression network analyses (WGCNA) identified only modules significantly associated with ELA (p≤0.05), not with SAD. Furthermore, analyzing interaction networks of the genes from the ELA-associated modules and the SAD-related MAPK3) revealed complex interactions of those genes. Gene functional enrichment analyses indicate a role of signal transduction pathways as well as inflammatory responses supporting an involvement of the immune system in the association of ELA and SAD. In conclusion, we did not identify a direct molecular link between ELA and adult SAD by transcriptional changes. However, our data indicate an indirect association of ELA and SAD mediated by the interaction of genes involved in immune-related signal transduction.
2023-04-16 | GSE228702 | GEO
Project description:Whereas the risk factors for structural valve deterioration (SVD) of glutaraldehyde (GA)- treated bioprosthetic heart valves (BHVs) are well-studied, those responsible for the failure of next-generation BHVs fixed with alternative chemicals remain largely unknown. Here, we collected 11 ethylene glycol diglycidyl ether (EGDE)-treated BHVs excised because of SVD and 5 calcified aortic valves (AVs) replaced with BHVs due to the calcific aortic valve disease (CAVD), further deciphering their proteomic profile.
2022-12-25 | PXD035113 | Pride
Project description:Social anxiety disorder (SAD) is a psychiatric disorder characterized by extensive fear in social situations. Multiple genetic and environmental factors are known to contribute to its pathogenesis. One of the main environmental risk factors is early life adversity (ELA). Evidence is emerging that epigenetic mechanisms such as DNA methylation might play an important role in the biological mechanisms underlying SAD and ELA. To investigate the relationship between ELA, DNA methylation, and SAD, we performed an epigenome-wide association study for SAD and ELA examining DNA from whole blood of a cohort of 143 individuals using DNA methylation arrays. We identified two differentially methylated regions (DMRs) associated with SAD located within the genes SLC43A2 and TNXB. As this was the first epigenome-wide association study for SAD, it is worth noting that both genes have previously been associated with panic disorder. Further, we identified two DMRs associated with ELA within the SLC17A3 promoter region and the SIAH3 gene and several DMRs that were associated with the interaction of SAD and ELA. Of these, the regions within C2CD2L and MRPL28 showed the largest difference in DNA methylation. Lastly, we found that two DMRs were associated with both the severity of social anxiety and ELA, however, neither of them was found to mediate the contribution of ELA to SAD later in life. Future studies are needed to replicate our findings in independent cohorts and to investigate the biological pathways underlying these effects.
2021-01-31 | GSE164056 | GEO