AhR activation by TCDD mobilized MDSCs from bone marrow to peritoneal cavity with immunosuppressive activity
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ABSTRACT:
ORGANISM(S): synthetic construct Mus musculus
PROVIDER: GSE134337 | GEO | 2019/07/31
REPOSITORIES: GEO
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Project description:AhR activation by TCDD mobilized MDSCs from bone marrow to peritoneal cavity with immunosuppressive activity
| PRJNA554799 | ENA
Project description:This study dermined the temporal gene expression profile of myeloid subpopulations recruited to the peritoneal cavity to encapsulate implanted foreign material. Sterile foreign objects were inserted into the peritoneal cavities of MacGreen mice (in which the Csf1r promoter directs myeloid-specific EGFP expression). At various time-points post-surgery (days 2, 4, 7, 14), mice were euthanased, and peritoneal exudate cells removed by lavage. Peritoneal exudate cells from MacGreen mice that had not received implants were used as controls (day 0; 'unstimulated'). Free-floating objects encapsulated with tissue were removed from the peritoneal cavities of different mice at days 7, 14, 21, 28 days, and single cell suspensions obtained by collagenase digestion. Single-cell suspensions from peritoneal exudate or tissue capsules were separated on the basis of size/granularity and EGFP fluorescence using FacsVantage SE Diva. Total RNA was extracted from FACS-sorted EGFP-hi cells.
2014-09-17 | E-GEOD-53101 | biostudies-arrayexpress
Project description:The effect of selected adjuvants on the mRNA expression of peritoneal exudate cells.
2009-09-23 | E-MEXP-1814 | biostudies-arrayexpress
Project description:2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminant. Previous reports revealed TCDD activating aryl hydrocarbon receptor (AhR) pathway and causing cardiac damage. However, the mechanism of AhR-induced cardiac defect in response to TCDD exposure remains unclear. In this study, we characterized the impacts of TCDD exposure on heart morphology and cardiac function in zebrafish. To investigate the differentially expressed genes under TCDD exposure, we collected the zebrafish larave heart from the control and TCDD treatment groups. We then performed gene expression profiling analysis using data obtained from RNA-seq. Transcriptomic profiling showed that, along with an upregulation of the AhR signaling pathway by TCDD, the expression of pro-ferroptosis genes was upregulated, while genes implicated in glutathione metabolism were downregulated. Consistently, lipid peroxidation, as indicated by malonaldehyde (MDA) production, increased in TCDD-exposed cardiac tissue. Accordingly, inhibiting lipid peroxidation with Liproxstatin-1 reversed the adverse cardiac effects under TCDD treatment. Together, our findings demonstrate that AhR-mediated lipid peroxidation contributes to the cardiac developmental defects of TCDD during zebrafish early development.
2022-10-30 | GSE206948 | GEO
Project description:The aryl hydrocarbon receptor (AHR) mediates most of the toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). However, TCDD toxicity phenotypes vary widely between species, strains and even between sexes within a strain. While the exact reasons for this variation remain unclear, it is thought to be related to differences in the structure of the AHR. Previous studies comparing the downstream effects of TCDD exposure between animals with different AHR isoforms have been confounded by the genetic differences between these model systems. To address this issue conclusively, we evaluated three transgenic mouse lines, each of which express a different rat AHR isoform (rWT, DEL, and INS) from two strains of rat with highly divergent TCDD-susceptibilities, within identical genetic backgrounds. Here we profile hepatic transcriptomic responses following exposure to TCDD, and use these to identify transcripts associated with toxicity. We have confirmed that the variation in toxicity is inherent to the AHR isoform. Additionally, we note the enhanced activity of the modified transactivation domain of the DEL isoform, relative to the INS isoform, and provide further evidence that the INS isoform is responsible for the high resistance to TCDD observed in H/W rats. We also uncover several candidate genes that were consistently differentially expressed in TCDD-sensitive mice and rats.
2016-01-01 | GSE72270 | GEO
Project description:We seeked to determine in vivo effects of IFNg and IFNa response in peritoneal cavity macrophages. These cells were part of ImmGen Interferon cytokine study and immunocytes were sorted according to Immgen's standard lineage panel. Profiles from peritoneal cavity macrophages were used to analyze cell specific responses to IFNg.
2018-02-14 | GSE110549 | GEO
Project description:The aryl hydrocarbon receptor (AHR) mediates most of the toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). However, TCDD toxicity phenotypes vary widely between species, strains and even between sexes within a strain. While the exact reasons for this variation remain unclear, it is thought to be related to differences in the structure of the AHR. Previous studies comparing the downstream effects of TCDD exposure between animals with different AHR isoforms have been confounded by the genetic differences between these model systems. To address this issue conclusively, we evaluated three transgenic mouse lines, each of which express a different rat AHR isoform (rWT, DEL, and INS) from two strains of rat with highly divergent TCDD-susceptibilities, within identical genetic backgrounds. Here we profile hepatic transcriptomic responses following exposure to TCDD, and use these to identify transcripts associated with toxicity. We have confirmed that the variation in toxicity is inherent to the AHR isoform. Additionally, we note the enhanced activity of the modified transactivation domain of the DEL isoform, relative to the INS isoform, and provide further evidence that the INS isoform is responsible for the high resistance to TCDD observed in H/W rats. We also uncover several candidate genes that were consistently differentially expressed in TCDD-sensitive mice and rats. Adult male transgenic mice were treated by gavage with 0, 125, 250, 500, or 1000 µg/kg TCDD dissolved in corn oil vehicle. Mice were euthanized 4 days following treatment and liver tissue was harvested for analysis. RNA was isolated and the transcriptome for each animal assayed on separate microarrays.
2016-07-03 | E-GEOD-72270 | biostudies-arrayexpress
Project description:ChIP-seq was done on cryopreserved primary human hepatocyte with vehicle control - 0.1% dimethylsulfide (DMSO), or 1nM 2,3,7,8 tetrachlorodibezno-p-dioxin (TCDD) agonist treatment to identify AHR binding regions throughout the genome. We identified 1,984 binding peaks when comparing TCDD vs. vehicle control
2022-06-09 | GSE205502 | GEO
Project description:Over activation of the aryl hydrocarbon receptor (AhR) by TCDD results ampng other phenotypes in severe thymic atrophy accompanied by immunosuppression. The link between thymic atrophy, skewed thymocyte differntiation and immunosuppression is still not fully resolved. This study investigates the TCDD elicted exprssion changes in the ET, cortical thymus epithelial cell line. Keywords: TCDD, AhR, thymic epithelial cells, thymic involution, thymus atrophy
2008-12-31 | GSE10168 | GEO
Project description:Exposure to environmental contaminants can disrupt normal development of the early vertebrate skeleton. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs craniofacial skeletal development across many vertebrate species and its effects are especially prominent in early life stages of fish. TCDD activates the aryl hydrocarbon receptor (AHR), a transcription factor that mediates most if not all TCDD responses. We investigated the transcriptional response in the developing zebrafish jaw following TCDD exposure using DNA microarrays. Zebrafish larvae were exposed to TCDD at 96 h postfertilization (hpf) and jaw cartilage tissue was harvested for microarray analysis at 1, 2, 4 and 12 h postexposure (hpe). Numerous chondrogenic transcripts were misregulated by TCDD in the jaw. Comparison of transcripts altered by TCDD in jaw with transcripts altered in embryonic heart showed that the transcriptional responses in the jaw and the heart were strikingly different. Sox9b, a critical chondrogenic transcription factor, was the most significantly reduced transcript in the jaw. We hypothesized that the TCDD reduction of sox9b expression plays an integral role in affecting formation of the embryonic jaw. Morpholino knock down of sox9b expression demonstrated that partial reduction of sox9b expression alone was sufficient to produce a TCDD-like jaw phenotype. Heterozygous sox9b deletion mutant embryos were sensitized to TCDD. Lastly, embryos injected with sox9b mRNA and then exposed to TCDD blocked TCDD-induced jaw toxicity in approximately 14% of sox9b-injected embryos. These results suggest that reduced sox9b expression in TCDD-exposed zebrafish embryos contributes to jaw malformation. Keywords: Time course
2008-11-01 | GSE11893 | GEO