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IEC intrinsic IL-1R signaling holds dual roles in regulating intestinal homeostasis and inflammation

ABSTRACT: IEC intrinsic IL-1R signaling holds dual roles in regulating intestinal homeostasis and inflammation

PROVIDER: PRJNA795516 | ENA |

REPOSITORIES: ENA

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IEC intrinsic IL-1R signaling holds dual roles in regulating intestinal homeostasis and inflammation

Project description:Introduction: Intestinal epithelial cells (IECs) constitute a critical first line of defense against microbes by providing a physical barrier capable of producing antimicrobial peptides (AMPs) and cytokines. While IECs are known to respond to various microbial signals, the precise upstream cues regulating diverse IEC responses are not clear. Method: Mouse intestinal crypts were isolated from colon tissue. Crypts were differentiated into 3D spheroids in matrigel by stimulating with LWRN media and growth factors. After differentiation colonoids were stimulated with IL-1b, IL-22, or IL-1b and IL-22 for 12 hours then RNA was isolated for RNA sequencing. Conclusion: Transcriptional profiling of mColonoids reveals IL-1b synergizes with IL-22 to induced a unique gene profile

2023-03-22 | GSE193267 | GEO

Expression data from jejunum IEC deleted for both HDAC1 and HDAC2

Project description:Both HDAC1 and HDAC2 are epigenetic erasers that drive specific and redundant gene expression patterns, in part by removing acetyl groups on histones. Deletion of these Hdac in intestinal epithelial cell (IEC) in vivo alters intestinal homeostasis, dependent on the Hdac deleted and the level of expression of both. To determine the intrinsic specific IEC function of HDAC1 and HDAC2, we have performed transcriptomic and quantitative proteomic approaches on IEC-deficient for Hdac1 and Hdac2. We have defined changes in both mRNA and protein expression patterns affecting IEC differentiation. We have identified IEC Hdac1- and Hdac2-dependent common as well as specific pathways and biological processes. These findings uncover unrecognized similarities and differences between normal IEC and HDAC1/2 deleted jejunum IEC.

2020-12-31 | GSE158522 | GEO

Expression profile of WT and IKKb(EE)IEC epithelial cells (IEC)

Project description:To investigate NF-kB-driven gene expression in IEC, we performed microarray analysis from enterocytes of mice that express a constitutively active form of IKKb in intestinal epithelial cells Total RNA was prepared from enterocytes obtained from small intestines of IKKb(EE)IEC and WT littermates. Two biological replicates were performed for each experimental condition.

2011-06-09 | E-GEOD-29701 | biostudies-arrayexpress

BI 456906: a dual glucagon-like peptide-1/glucagon agonist promoting bodyweight reduction

Project description:Glucagon and glucagon-like peptide-1 (GLP-1) are hormones involved in energy homeostasis. GLP-1 receptor (GLP-1R) agonism reduces food intake and delays gastric emptying, and glucagon receptor (GCGR) agonism increases energy expenditure by thermogenesis. BI 456906 is a subcutaneous, once-weekly injectable dual GLP-1R/GCGR agonist in development for the treatment of obesity or non-alcoholic steatohepatitis. Here we show that BI 456906 is a potent dual agonist with an extended half-life in human plasma. Key GLP-1R-mediated mechanisms of reduced food intake, delayed gastric emptying and improved glucose tolerance were confirmed in GLP-1R knockout mice. GCGR activity was confirmed by reduced plasma amino acids, increased hepatic expression of nicotinamide N-methyltransferase and increased energy expenditure. BI 456906 produced greater bodyweight reductions than maximally efficacious semaglutide doses and modulated gene expression, including genes involved in amino acid metabolism. BI 456906 is a potent dual agonist that produces bodyweight-lowering effects through both GLP-1R and GCGR agonism.

2022-12-09 | GSE211105 | GEO

Knockdown IGF-1R triggers viral RNA sensors MDA5- and RIG-1-mediated the mitochondrial apoptosis in colonic cancer cells

Project description:The important role of IGF-1R in cancers has been well established. Classical model involves IGF-1/2 binding to IGF-1R, following activation of the PI3K/Akt pathway, thereby promoting cell proliferation, apoptosis inhibition and treatment resistance. While IGF-1R has become a promising target for cancer therapy, clinical disclosures subsequently have been less encouraging. The question is whether targeting IGF/IGF-1R still holds therapeutic potential. Here we show a novel mechanism that knockdown IGF-1R surprisingly triggers cytoplasmic viral RNA sensors MDA5 and RIG-1, leading to mitochondrial apoptosis in cancer. We analyzed MDA5 and RIG-1 in the intestinal epithelium of IGF-1R knockdown mice. Igf1r+/- mice demonstrated higher MDA5 and RIG-1 than WT mice. IGF-1R knockdown-triggered MDA5 and RIG-1 was further analyzed in human cancer and normal cells. Increased MDA5 and RIG-1 were clearly seen in the cytoplasm identified by immunofluoresce in the cells silenced IGF-1R. Block off IGF-1R downstream PI3K/Akt did not impact on MDA5 and RIG-1 expression. IGF-1R knockdown-triggered MDA5 and RIG-1 and their signaling pathways were similar to those of viral RNA mimetic poly(I:C) had. IGF-1R knockdown-triggered MDA5 and RIG-1 led to cancer apoptosis through activation of the mitochondrial pathway. In vivo assay, Igf1r+/- mice strongly resisted AOM-induced colonic tumorigenesis through triggering MDA¬5- and RIG-1-mediated apoptosis. Notably, RIG-I and MDA5-mediated proapoptotic signaling pathway is preferential active in cancer cells. These data suggest that targeting IGF-1R-triggered MDA5 and RIG-1 might have therapeutic potential for cancer treatment.

2019-11-30 | GSE122534 | GEO

Dual T cell– and B cell–intrinsic deficiency in humans

Project description:Dual T cell– and B cell–intrinsic deficiency in humans

| PRJNA716960 | ENA

Expression data from ileum samples from FADD IEC-KO (intestinal epithelial cell-knock out) and CASP8 IEC-KO mice in combination with different genetic mutations (Zbp1 -/-, Mlkl -/-, Ripk3 IEC-KO)

Project description:FADD-IEC KO and CASP8 IEC-KO mice spontaneously develop chronic ileitis charcterized by inflammatory gene expression. We characterized the role of MLKL, RIPK3, ZBP1, in the upregulation of inlflammatory genes in these mice. We used microarray to study the effect of MLKL, RIPK3 and ZBP1 on the gene expression profile in FADD IEC-KO and/or CASP8 IEC-KO mice and detect effects on specific inflammatory genes.

2020-05-01 | GSE137280 | GEO

Expression data from colon samples from FADD IEC-KO (intestinal epithelial cell-knock out) and CASP8 IEC-KO mice in combination with different genetic mutations (Zbp1 -/-, Mlkl -/-, Ripk3 IEC-KO)

Project description:FADD-IEC KO and CASP8 IEC-KO mice spontaneously develop chronic colitis charcterized by inflammatory gene expression. We characterized the role of MLKL, RIPK3, ZBP1, in the upregulation of inlflammatory genes in these mice. We used microarray to study the effect of MLKL, RIPK3 and ZBP1 on the gene expression profile in FADD IEC-KO and/or CASP8 IEC-KO mice and detect effects on specific inflammatory genes.

2020-05-01 | GSE137281 | GEO

BulkRNA sequencing of small intestinal IEC epithelial cells of Casp3/7ΔIEC mice and Casp3/7FL/FL littermates

Project description:Apoptosis is widely believed to be crucial for epithelial cell death and shedding in the intestine, thereby shaping the overall architecture of the gastrointestinal tract, but also regulating tolerance induction during homeostasis. To experimentally address this concept, we generated intestinal epithelial cell (IEC)-specific knockout mice that lack both executioner caspase-3 and caspase-7 (Casp3/7?IEC), which are the converging point of the extrinsic and intrinsic apoptotic pathway. Surprisingly, the overall architecture, cellular landscape and proliferation rate remained unchanged in these mice. However, non-apoptotic cell extrusion was increased in Casp3/7?IEC mice, compensating apoptosis deficiency, maintaining the same physiological level of IEC shedding. Microbiome richness and composition stayed unaffected, bearing no sign of dysbiosis. Transcriptome and single cell RNA sequences analyses of IECs and immune cells revealed no differences in signaling pathways of differentiation and inflammation. These findings demonstrate that during homeostasis apoptosis per se is dispensable for IEC turnover at the top of intestinal villi intestinal tissue dynamics, microbiome composition and immune regulation.

2022-01-01 | GSE183811 | GEO

Expression profile of WT and IKKb(EE)IEC epithelial cells (IEC)

2011-06-09 | GSE29701 | GEO