FoxO4 ChIP-Seq profiles of WT differentiated TH1 cells
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ABSTRACT:
PROVIDER: PRJNA549721 | ENA |
REPOSITORIES: ENA
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Project description:This study is to analyze genome-wide occupancy of FoxO4 in WT TH1 cells.
2020-06-19 | GSE133034 | GEO
Project description:To assess the function of FoxO4 in processes of TH1 differentiation, we have performed a whole genome microarray assay to discover the significant changed genes in normal and FoxO4 overexpressing TH1 cells.
2020-06-19 | GSE133033 | GEO
Project description:Gene expression profiles of FoxO4 overexpressing TH1 cells.
| PRJNA549722 | ENA
Project description:Forkhead box O transcriptional factors, especially FoxO1 and FoxO3a, play critical roles in physiologic and pathologic immune responses. Here, in studies to explore the function of FoxO4 in lymphocyte biology, we showed that loss of FoxO4 in T cells promotes TH1 cell differentiation and augments the production of interferon-γ (IFN-γ) in vitro. Correspondingly, conditional deletion of FoxO4 in CD4+ T cells enhances T cell-specific responses to Listeria monocytogenes infection in vivo. Genome-wide occupancy and transcriptomic analyses identified DKK3 (encoding Dickkopf-3 protein) as a direct transcriptional target gene of FoxO4. Consistent with the FoxO-DKK3 relationship, recombinant DKK3 protein restored normal levels of IFN-γ production in FoxO4-deficient TH1 cells, through downregulation of Lef1 expression. Together, our data identify and validate a novel FoxO4-DKK3-LEF-1 axis in TH1 cell differentiation, providing an important insight and supplement for FoxO family proteins in T lymphocyte biology, and revealing a promising target for treatment of immune-related diseases.
2020-06-19 | GSE133035 | GEO
Project description:Analysis of mechano-regulation of tenocyte metabolism at gene expression level. The hypothesis tested in the present study was that cyclic tensile strain influence the balance of anabolism/catabolism of tenocytes. Forkhead box O (FoxO) proteins are a family of transcription factors implicated in many biological processes including immune regulation. In this study, we found that mice null for Foxo4, a member of the FoxO family, are more susceptible to 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis than wild type controls. To understand the mechanism of elevated colitis susceptibility and the nature of the TNBS-induced colitis in Foxo4-null mice, we performed microarray analysis with mucosal cDNA samples from large intestines of untreated, ethanol and TNBS-treated wild type and Foxo4 KO mice. Unexpectedly, we found that cytokine CCL5, CXCL9, TNFalpha, and IFNgamma were already significantly upregulated in untreated Foxo4-null mice compared to WT controls despite lack of visible colonic phenotypes. Consistent with the exacerbated inflammatory phenotype in TNBS-treated Foxo4 KO mice, expressions of these inflammatory cytokines are further upregulated after TNBS-treatment. In addition, we observed many more inflammatory cytokines that were upregulated in TNBS-treated Foxo4 KO mice, including chemokines (CCL3, 4, 7, 8, 11, 12, 21b and CXCL1, 12, 14), chemokine receptors (CCR7, CCRl2, 8,CXC3CR1), cytokines (IL-1, IL-6, IL-11, IFI205), and cytokine receptors (TNFrsf). Interestingly, many of the anti-bacterial peptides were also up-regulated in TNBS treated Foxo4 KO mice including defensin related cryptdin (Defcr3,5,6, 9,13) and Defcr related sequence (Defcr-cr1,2,10,12). Up-regulation of basal level of IFNgamma, TNFalpha, CCL5, and CXCL9 expression in Foxo4 KO mice is specific to colonic tissues, as no significant difference of these gene transcript levels between wild type and Foxo4 KO mice was observed in other tissues including thymus . IFNgamma, TNFalpha, and IL-1ï¢which are upregulated in TNBS-treated Foxo4 KO mice, are Th1 type cytokines. This is consistent with the Th1 inflammatory phenotype observed in TNBS-treated Foxo4-KO mice. We also tested whether the expression of Th2 cytokines (IL-4, IL-5, and IL-13) is altered in TNBS-treated WT and Foxo4-null mice in comparison to ethanol-treated mice and observed no significant differences suggesting that the TNBS-induced colitis in Foxo4-null FVB mice is predominantly Th1 in nature. Colonic mucosal tissues from five mice per treatment group (untreated, two days after ethanol or TNBS-treatment) were pooled. Total RNA obtained from colon mucosa isolated tendon fascicles subjected to 1 or 24 hours in vitro cyclic tensile strain compared to unstrained control fascicles.
2010-05-28 | E-GEOD-16033 | biostudies-arrayexpress
Project description:Analysis of mechano-regulation of tenocyte metabolism at gene expression level. The hypothesis tested in the present study was that cyclic tensile strain influence the balance of anabolism/catabolism of tenocytes. Forkhead box O (FoxO) proteins are a family of transcription factors implicated in many biological processes including immune regulation. In this study, we found that mice null for Foxo4, a member of the FoxO family, are more susceptible to 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis than wild type controls. To understand the mechanism of elevated colitis susceptibility and the nature of the TNBS-induced colitis in Foxo4-null mice, we performed microarray analysis with mucosal cDNA samples from large intestines of untreated, ethanol and TNBS-treated wild type and Foxo4 KO mice. Unexpectedly, we found that cytokine CCL5, CXCL9, TNFalpha, and IFNgamma were already significantly upregulated in untreated Foxo4-null mice compared to WT controls despite lack of visible colonic phenotypes. Consistent with the exacerbated inflammatory phenotype in TNBS-treated Foxo4 KO mice, expressions of these inflammatory cytokines are further upregulated after TNBS-treatment. In addition, we observed many more inflammatory cytokines that were upregulated in TNBS-treated Foxo4 KO mice, including chemokines (CCL3, 4, 7, 8, 11, 12, 21b and CXCL1, 12, 14), chemokine receptors (CCR7, CCRl2, 8,CXC3CR1), cytokines (IL-1, IL-6, IL-11, IFI205), and cytokine receptors (TNFrsf). Interestingly, many of the anti-bacterial peptides were also up-regulated in TNBS treated Foxo4 KO mice including defensin related cryptdin (Defcr3,5,6, 9,13) and Defcr related sequence (Defcr-cr1,2,10,12). Up-regulation of basal level of IFNgamma, TNFalpha, CCL5, and CXCL9 expression in Foxo4 KO mice is specific to colonic tissues, as no significant difference of these gene transcript levels between wild type and Foxo4 KO mice was observed in other tissues including thymus. IFNgamma, TNFalpha, and IL-1beta, which are upregulated in TNBS-treated Foxo4 KO mice, are Th1 type cytokines. This is consistent with the Th1 inflammatory phenotype observed in TNBS-treated Foxo4-KO mice. We also tested whether the expression of Th2 cytokines (IL-4, IL-5, and IL-13) is altered in TNBS-treated WT and Foxo4-null mice in comparison to ethanol-treated mice and observed no significant differences suggesting that the TNBS-induced colitis in Foxo4-null FVB mice is predominantly Th1 in nature.
2010-05-12 | GSE16033 | GEO
Project description:We report the differential mRNA expressino of WT and Chi3l1 KO Th1 cells. We cultured WT and Chi3l1 KO naive CD4 T cells under Th1 skewing condition : plate-bound anti-CD3/28 antibody (2ug/mL), IL-12 0.2ng/mL, IL-2 50U/mL, anti-IL-4 neutralizing antibody 2ug/mL, for 3 days. We found different Th1 regulatory and tumoricidal-related gene expression in Chi3l1 KO T cells.
2018-02-13 | GSE105056 | GEO
Project description:RNA-sequencing of in vitro differentiated WT and Chi3l1 KO Th1 cell
| PRJNA414488 | ENA
Project description:AKT1 is a serine/threonine kinase implicated in fetal, placental, and postnatal growth. In this study, we investigated roles for AKT1 in placental development using a genome-edited/loss-of-function rat model. Both heterozygous and homozygous Akt1 mutant rats were viable and fertile. Disruption of AKT1 resulted in placental, fetal, and postnatal growth restriction. Akt1 null placentas showed deficits in both junctional zone and labyrinth zone size and their ability to adapt to a physiological stressor. Robust differences in the transcriptome of wild type versus Akt1 null junctional zones were identified. Among the differentially expressed junctional zone transcripts was forkhead box O4 (Foxo4), which encodes a transcription factor and known AKT substrate. FOXO4 expression was prominent in the junctional zone and invasive trophoblast cells of the rat placentation site and enhanced following rat TS cell differentiation. Foxo4 gene disruption using genome-editing resulted in placentomegaly, including an enlarged junctional zone. AKT1 and FOXO4 regulate the expression of many of the same transcripts expressed by trophoblast cells; however, in opposite directions. In summary, we have identified AKT1 and FOXO4 as part of a regulatory network controlling hemochorial placenta development.
2023-01-05 | GSE205829 | GEO
Project description:AKT1 is a serine/threonine kinase implicated in fetal, placental, and postnatal growth. In this study, we investigated roles for AKT1 in placental development using a genome-edited/loss-of-function rat model. Both heterozygous and homozygous Akt1 mutant rats were viable and fertile. Disruption of AKT1 resulted in placental, fetal, and postnatal growth restriction. Akt1 null placentas showed deficits in both junctional zone and labyrinth zone size and their ability to adapt to a physiological stressor. Robust differences in the transcriptome of wild type versus Akt1 null junctional zones were identified. Among the differentially expressed junctional zone transcripts was forkhead box O4 (Foxo4), which encodes a transcription factor and known AKT substrate. FOXO4 expression was prominent in the junctional zone and invasive trophoblast cells of the rat placentation site and enhanced following rat TS cell differentiation. Foxo4 gene disruption using genome-editing resulted in placentomegaly, including an enlarged junctional zone. AKT1 and FOXO4 regulate the expression of many of the same transcripts expressed by trophoblast cells; however, in opposite directions. In summary, we have identified AKT1 and FOXO4 as part of a regulatory network controlling hemochorial placenta development.
2023-01-05 | GSE205828 | GEO