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RNA sequencing of CD4+ T cells from mice developmentally exposed to TCDD

ABSTRACT: RNA sequencing of CD4+ T cells from mice developmentally exposed to TCDD

PROVIDER: PRJNA554357 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9677270.fastq.gz	Fastqsanger.gz
	SRR9677271.fastq.gz	Fastqsanger.gz
	SRR9677272.fastq.gz	Fastqsanger.gz
	SRR9677273.fastq.gz	Fastqsanger.gz
	SRR9677274.fastq.gz	Fastqsanger.gz

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RNA sequencing of CD4+ T cells from mice developmentally exposed to TCDD

Project description:We used next generation RNAsequencing to identify how triggering the aryl hydrocarbon receptor (AHR) during development alters T cell gene expression. Specifically, mice were developmentally exposed to vehicle or the AHR agonist TCDD. At adulthood, mice were infected with influenza A virus. CD44hiCD4+ and CD44loCD4+ T cells were FACs purified from the mediastinal lymph nodes on day 9 post infection. RNA was isolated from these cells, and RNA-seq was performed. Gene expression analysis revealed developmental AHR activation durably changes the expression of genes involved in several important CD4+ T cell functions, including proliferation, differentiation, and metabolism.

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RNA-sequencing of CD4+ T cells from mice prior to and after infection with influenza virus, and that were exposed developmentally to vehicle or TCDD

Project description:We used next generation RNAsequencing to identify how developmental exposure to TCDD alters gene expression in CD4+ T cells. Specifically, mice were developmentally exposed to vehicle or TCDD. At adulthood, CD4+ T cells were purified from peripheral lymph nodes of naive animals or the mediastinal lymph nodes of influenza A virus (IAV) infected mice (9 days post infection). RNA was isolated from these cells, and RNA-seq was performed. Gene expression analysis revealed developmental activation of the aryl hydrocarbon receptor with TCDD changes expression of genes that are involved in important CD4+ T cell functions.

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Whole Genome Bisulfite Sequencing of CD4+ T cells from mice developmentally exposed to vehicle or TCDD prior to and during influenza infection

Project description:We used Whole Genome Bisulfite Sequencing (WGBS) to compare DNA methylation patterns across the genome of CD4+ T cells. Specifically, mice were developmentally exposed to vehicle or TCDD. At adulthood, CD4+ T cells were purified from peripheral lymph nodes of naive animals or the mediastinal lymph nodes of influenza A virus (IAV) infected mice (9 days post infection). DNA was isolated from these cells, and WGBS was performed. Differential DNA methylation analyses revealed that both developmental exposure and IAV infection influence the pattern of DNA methylation in CD4+ T cells.

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Whole Genome Bisulfite Sequencing of CD4+ T cells from mice developmentally exposed to vehicle or TCDD prior to and during influenza infection

Project description:Whole Genome Bisulfite Sequencing of CD4+ T cells from mice developmentally exposed to vehicle or TCDD prior to and during influenza infection

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RNA-sequencing of CD4+ T cells from mice prior to and after infection with influenza virus, and that were exposed developmentally to vehicle or TCDD

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Project description:Comparison of expression profiles detected in A549 cells exposed to DMSO, TCDD, CH223191 or their combination Exposure to persistent ligands of aryl hydrocarbon receptor (AhR) has been found to cause lung cancer in experimental animals and lung adenocarcinomas are often associated with enhanced AhR expression and aberrant AhR activation. In order to better understand the action of toxic AhR ligands in lung epithelial cells, we performed global gene expression profiling in order to analyse TCDD- induced changes in A549 transcriptome, both sensitive and non-sensitive to co-treatment with AhR inhibitor CH223191. Comparison of our data with results from previously reported microarray and ChIP-seq experiments enabled us i) to identify candidate genes, which expression status acutely (e.g. Aldh1a3, Grem1, Hipk2, Tiparp), or with a delay (Cdh1, Dkk1, Bmp6), reflects exposure of lung cancer cells to TCDD, ii) to predict processes/pathways (e.g. ER stress, Wnt/β-cat, IFNɣ, EGFR/Erbb1), as well as iii) putative TFs (e.g. Stat, AP1, E2F1, TCF4), which may be implicated in adaptive response of lung cells to TCDD-induced AhR activation.

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