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Claudin-based barrier differentiation in the colonic epithelial crypt niche involves Hopx/Klf4 and Tcf7l2/Hnf4-alpha cascades

ABSTRACT: Analysis of the complex expression of claudin genes and transcription factors during intestinal epithelial cell differentiation across the crypt-to-surface colonic axis. Characterization of the complex expression gradients of transcription factors Hopx, Hnf4a, Klf4 and Tcfl2 and 12 claudin genes. In vitro confirmatory methods identified two pathways that stimulate claudin expression; Hopx/Klf4 activation of Cldn4, 7 and 15, and Tcf7l2/Hnf4a upregulation of Cldn23. Chromatin Immunoprecipitation confirmed a Tcf7l2/Hnf4a/Claudin23 cascade. Hnf4a conditional knockout mice fail to induce Cldn23 during colonocyte differentiation. The distal colon tissue was obtained from 4 male, 10-12 week old, C57BL/6 (WT) mice. The Arcturus Laser Capture Microdissection (LCM) system (Applied Biosystems/Life Technologies) was used to isolate crypt-base and surface cell populations providing two samples per mouse (crypt-base and surface). This resulted in 8 total samples for microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Loukia Lili

PROVIDER: E-GEOD-84742 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Claudin-based barrier differentiation in the colonic epithelial crypt niche involves Hopx/Klf4 and Tcf7l2/Hnf4-alpha cascades

Project description:Analysis of the complex expression of claudin genes and transcription factors during intestinal epithelial cell differentiation across the crypt-to-surface colonic axis. Characterization of the complex expression gradients of transcription factors Hopx, Hnf4a, Klf4 and Tcfl2 and 12 claudin genes. In vitro confirmatory methods identified two pathways that stimulate claudin expression; Hopx/Klf4 activation of Cldn4, 7 and 15, and Tcf7l2/Hnf4a upregulation of Cldn23. Chromatin Immunoprecipitation confirmed a Tcf7l2/Hnf4a/Claudin23 cascade. Hnf4a conditional knockout mice fail to induce Cldn23 during colonocyte differentiation.

2016-07-23 | GSE84742 | GEO

Mus musculus

Project description:Claudin-based barrier differentiation in the colonic epithelial crypt niche involves Hopx/Klf4 and Tcf7l2/Hnf4-alpha cascades

| PRJNA330979 | ENA

Chromatin occupancy and target genes of TCF7L2 in hepatocytes

Project description:TCF7L2 regulates multiple metabolic pathways in hepatocytes through a transcriptional network involving HNF4M-NM-1 For the identification of Tcf7l2 target genes using a RNA-seq timecourse, and for identifying the binding sites of Tcf7l2 and Hnf4a, Tcf7l2 was silenced in rat H4IIE hepatocytes using siRNA for Tcf7l2 with a scrambled siRNA as control. Treatment times for RNA-seq samples were 3, 6, 9, 12, 15, 18, 48, and 96 hours, and for ChIP-seq samples 15 h. RNA-seq timecourse was performed in duplicate or triplicate, and the ChIP-seq in duplicate for Tcf7l2 and in singlicate for Hnf4a. The H4IIE-specific transcriptome was defined from an independent set of pooled 24 h siRNA treated samples (N=3 for siRNA for Tcf7l2 and N=3 for scrambled siRNA).

2014-11-24 | E-GEOD-53862 | biostudies-arrayexpress

The Tight Junction Protein Claudin-2 Controls Mucosal Permeability, Immune Tolerance and Colitis in Mice

Project description:The mucosal epithelium plays a key role in regulating immune homeostasis. Dysregulation of epithelial barrier function is associated with mucosal inflammation. Expression of claudin-2, a pore-forming tight junction protein, is highly upregulated during inflammatory bowel disease (IBD) and, due to its association with epithelial permeability, has been postulated to promote inflammation. Furthermore, claudin-2 also regulates colonic epithelial cell proliferation and intestinal nutrient absorption. However, the precise role of claudin-2 in regulating colonic epithelial and immune homeostasis remains unclear. Here, we demonstrate, using Villin-Claudin-2 transgenic (Cl-2TG) mice, that increased colonic claudin-2 expression unexpectedly protects mice against experimentally induced colitis and colitis-associated cancer. Notably, Cl-2TG mice exhibited increased colon length and permeability as compared with wild type (WT) littermates. However, despite their leaky colon, Cl-2TG mice subjected to experimental colitis were immune compromised, with reduced induction of TLR-2, TLR-4, Myd-88 expression and NF-kB and STAT3 activation. Most importantly, colonic macrophages in Cl-2TG mice exhibited an anergic phenotype. Claudin-2 overexpression also increased colonocyte proliferation and provided protection against colitis-induced colonocyte death. Taken together, our findings have revealed a critical role of claudin-2 in regulating colonic homeostasis, suggesting novel therapeutic strategies for inflammatory conditions of the gastrointestinal tract. 8-10 weeks old male Villin-Claudin-2 transgenic mice and WT littermates were provided either normal drinking water (control) or Dextran Sodium Sulfate (DSS: 4% w/v) for 10 days. 3 replicates each.

2013-09-15 | E-GEOD-46006 | biostudies-arrayexpress

The Tight Junction Protein Claudin-2 Controls Mucosal Permeability, Immune Tolerance and Colitis in Mice

2013-09-15 | GSE46006 | GEO

ena-DATASET-UH-tumor-30-04-2018-10:14:30:708-124 - samples

Project description:Chip-exo and Chip-nexus for FOXA1, HNF4A, KLF5, MYC, and TCF7L2 in colorectal cancer cell lines LoVo, GP5D, COLO320DM

| EGAD00001004099 | EGA

The role of TCF7L2 rs290487 variant in hepatic glucose metabolism: an integrated analysis of clinical and multi-omics data

Project description:TCF7L2 rs290487 C allele increases diabetic risk in Chinese, however the mechanism remains unclear. We herein evaluated the role of rs290487 variant in hepatic glucose homeostasis by integrating clinical and multi-omics data (ChIP-seq, ATAC-seq, RNA-seq, and metabolomics) from CRISPR/Cas9 edited PLC-PRF-5 cell lines (C/C vs. C/T). In clinical cohort, C/C genotype was associated with higher insulin resistance index and higher incidence of hepatogenous diabetes as compared to C/T heterozygote and T/T homozygote genotypes. In liver cell lines, C/C-cells had enhanced glucose production and lower TCF7L2 mRNA and protein levels than C/T-cells. Moreover, C/C-cells presented specific binding affinity of TCF7L2 with genes involving glucose metabolism (e.g., PFKP and PPARGC1A), increased expression of gluconeogenetic genes with specific chromatin openness (e.g., PPARGC1A and HNF4A), and deregulation of metabolites (e.g., β-D-Fructose 2,6-bisphosphate). In addition, diabetic status (high glucose and insulin) had a more potent effect on TCF7L2 expression than the genetic variant, indicating a significant role of environmental factors on gene expression and disease progression. This study provides a novel mechanism underlying the association between TCF7L2 rs290487 polymorphism and hepatic regulation of glucose homeostasis.

2020-07-29 | GSE138781 | GEO

Gene expression profiles of normal human tonsillar cell subpopulations FACS sorted based on expression of cell surface markers

Project description:To characterize the progenitor-enriched CD44+NGFR+ cells present in the crypt and surface regions of the tonsil, we used an Illumina array system to analyze the transcriptome of these cells isolated from the tonsillar crypt and surface regions of three different individuals as well as the total epithelial (CD45-CD31-) populations obtained from two of these.

2015-10-29 | GSE69767 | GEO

IL-22+ T cells protect intestinal crypts from bacterial invasion and epithelial damage.

Project description:Three subsets of intestinal epithelial cells (IECs) (P9, Surface; P10, Large Crypt; P11, Small Crypt) were isolated from Naïve and Day 9 C.r.-infected Cntrl (Cre-) and CD4 cre+. Il22 floxed mice (CD4 cKO)

2023-05-30 | GSE114338 | GEO

Persistence of effector memory Th1 cells is regulated by the homeobox only protein Group1 Hopx-/-, Group2 Hopx+/-, Group3 Hopx+/+

Project description:Hopx appears to be needed for persistence of Th1 effector memory cells. IFN-gamma-producing Th cells are significantly reduced in Hopx-deficient mice compared to Hopx-expressing littermates and Hopx-deficient Th1 cells show a defective persistence upon adoptive transfer. Moreover, Hopx protects Th1 cells from Fas-mediated cell death in vitro. To further dissect the role of Hopx and to identify target genes of Hopx, we have performed transcriptome analysis to compare gene expression in Hopx-deficient versus Hopx-competent Th1 cells. In agreement with the role of Hopx in supporting survival of Th1 effector memory cells, anti-apoptotic cells were up-regulated and pro-apoptotic genes were down-regulated in Hopx-competent compared to Hopx-deficient Th1 cells.

2010-09-30 | GSE24437 | GEO

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