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RNA sequencing of intestinal enterocytes pre- and post-Roux-en-Y gastric bypass reveals alteration in gene expression related to enterocyte differentiation, restitution, and obesity

ABSTRACT: Background: The intestinal lining renews itself in a programmed fashion that can be affected by adaptation to surgical procedures such as gastric bypass. Results: RNA sequencing suggested significant decreases of gene expression associated with G2/M DNA damage checkpoint regulation of the cell cycle pathway, and significant increases in gene expression associated with CDP-diacylglycerol biosynthesis pathway TCA cycle II pathway, and pyrimidine ribonucleotide salvage pathway after RYGB. Since SLFN12 is reported to influence enterocytic differentiation, we stained mucosa for SLFN12 and observed increased SLFN12 immunoreactivity. We investigated SLFN12 overexpression in HIEC-6 and FHs 74 Int intestinal epithelial cells and observed similar increased expression of the following genes that were also increased after RYGB: HES2, CARD9, SLC19A2, FBXW7, STXBP4, SPARCL1, and UTS. Conclusions: Our data suggests that RYGB promotes SLFN12 protein expression, cellular mechanism and replication pathways, and genes associated with differentiation and restitution (HES2, CARD9, SLC19A2) and obesity-related genes (FBXW7, STXBP4, SPARCL1, UTS).

ORGANISM(S): Homo sapiens

PROVIDER: GSE214758 | GEO | 2022/11/01

REPOSITORIES: GEO

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Colon gene expression signatures in wild type and Card9-/-mice exposed to DSS induced colitis

Project description:It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. For the induction of colitis, mice were given drinking water supplemented with 2% (w/v) Dextran sulphate sodium (DSS) for 7 days, then allowed to recover by drinking water alone for 5 additional days. 3 mice of each groups (WT and Card9-/-) were sacrified before DSS administration. 5 WT mice and 4 Card9-/- mice were sacrified 7 days after DSS administration and 5 mice of each group were sacrified at day 12.

2016-04-05 | E-GEOD-67577 | biostudies-arrayexpress

HNF-1alpha Triggers Initiation of the Human Intestinal Cell Differentiation Program in Cooperation with Cdx-2 and GATA-4

Project description:Transcriptional profiling of undifferentiated HIEC cells stably infected with a retroviral inducible expression vector (RevTet system) comparing DOX-induced HIEC pTetON with DOX-induced HIEC cells expressing either HNF1 and CDX2 or HNF1, CDX2 plus GATA4. Keywords: Differential gene expression Three-condition experiment, DOX-induced HIEC expressing HNF1-CDX2 vs DOX-induced HIEC pTetON, DOX-induced HIEC expressing HNF1-CDX2 plus GATA4 vs DOX-induced HIEC pTetON.

2010-01-28 | E-GEOD-11421 | biostudies-arrayexpress

CARD9 impacts colitis by altering gut microbiota metabolism of tryptophan into aryl hydrocarbon receptor ligands

Project description:It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. Results published in Nature Medicine, doi:10.1038/nm.4102

2016-04-05 | GSE67577 | GEO

Expression data from RKO cells transfected with SPARCL1 and vector control

Project description:Colon cancer cell line RKO grown on Matrigel form a luminal-like structure after the transfection of SPARCL1 gene, which may imply the differentiation of the cells. To indentify genes regulated by SPARCL1, we built two stable cell lines: RKO with pLXSN-SPARCL1 plasmid (RKO-SPARCL1) and RKO with pLXSN plasmid (RKO-pLXSN). Then we cultured these two cell lines on both plastic dish and dish cover with a layer of Matrigel. We used microarrays to undentify global gene expression change in RKO cells after the tranfection of SPARCL1. Four samples including RKO-pLXSN cells cultured on plastic, RKO-pLXSN cells cultured on Matrigel, RKO-SPARCL1 cells cultured on plastic and RKO-SPARCL1 cells cultured on Matrigel were trypsinized and collected for RNA extraction and hybridization on Affymetrix microarray U133plus2.0. Supplementary files: * RLvsRP: up and down regulated genes comparing with RKO-SPARCL1(RL) and RKO-pLXSN(RP) cells cultured on plastic * RLMvsRPM: up and down regulated genes comparing with RKO-SPARCL1(RL) and RKO-pLXSN(RP) cells cultured on Matrigel

2011-09-29 | E-GEOD-31440 | biostudies-arrayexpress

HNF-1alpha Triggers Initiation of the Human Intestinal Cell Differentiation Program in Cooperation with Cdx-2 and GATA-4

2010-01-29 | GSE11421 | GEO

Cecum gene expression signatures in germ-free WT mice colonized with microbiota from WT or Card9-/- mice and infected with Citrobacter rodentium induced colitis

Project description:It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9-/- mice are more susceptible to colitis induced by Citrobacter rodentium as a result of impaired of the IL-22 pathway. C. rodentium is a natural mouse pathogen widely used to model human infections with Enteropathogenic Escherichia coli and Enterohaemorrhagic E. coli. To explore the role of the gut microbiota in the susceptibility of Card9-/- mice to C. rodentium infection, we colonized WT germ-free (GF) mice with the microbiota of WT (WT-->GF) or Card9-/- (Card9-/- -->GF) mice and challenged them with C. rodentium. Card9-/- -->GF mice were more susceptible than WT-->GF mice to C. rodentium. To examine the mechanisms responsible for this defect, we compared the cecum transcriptomes of WT -->GF and Card9-/- -->GF mice before and during C. rodentium-induced colitis. The number of down-regulated and up-regulated genes on day 12 after C. rodentium infection was lower in Card9-/- -->GF mice than WT-->GF mice. Card9-/- -->GF mice showed a significant down-regulation of gut morphogenesis and wound healing pathways suggesting that recovery is impaired in Card9-/- -->GF mice after C. rodentium infection. Immune response and cell division pathways were up-regulated in WT-->GF mice but not in Card9-/- -->GF confirming the defect of global response to infection when only the Card9-/- microbiota was transferred. The most induced and differentially expressed genes between Card9-/- -->GF and WT-->GF mice on day 4 after C. rodentium infection were Reg3g (encoding REGIIIγ) and Reg3b (encoding REGIIIβ).

2017-11-25 | GSE90577 | GEO

Velcrin-induced selective cleavage of tRNALeu(TAA) by SLFN12 causes cancer cell death [tRNA seq]

Project description:Velcrin compounds kill cancer cells expressing high levels of phosphodiesterase 3A (PDE3A) and Schlafen family member 12 (SLFN12) by inducing complex formation between these two proteins, but the mechanism of cancer cell killing by the PDE3A–SLFN12 complex is not fully understood. Here, we report that the physiological substrate of SLFN12 RNase is tRNALeu(TAA). SLFN12 selectively digests tRNALeu(TAA), and velcrin treatment promotes the cleavage of tRNALeu(TAA) by inducing PDE3A–SLFN12 complex formation in vitro. We found that distinct sequences in the variable loop and acceptor stem of tRNALeu(TAA) are required for substrate digestion. Velcrin treatment of sensitive cells results in downregulation of tRNALeu(TAA), ribosome pausing at Leu-TTA codons and global inhibition of protein synthesis. Velcrin-induced cleavage of tRNALeu(TAA) by SLFN12 and the concomitant global inhibition of protein synthesis thus define a new mechanism of apoptosis initiation.

2022-09-01 | GSE185827 | GEO

Velcrin-induced selective cleavage of tRNALeu(TAA) by SLFN12 causes cancer cell death [Ribo-Seq]

2022-09-01 | GSE185826 | GEO

Velcrin-induced selective cleavage of tRNALeu(TAA) by SLFN12 causes cancer cell death [RNA-Seq]

2022-09-01 | GSE185822 | GEO

Vav proteins are key regulators of Card9 signaling for innate antifungal immunity

Project description:Fungal infections are major causes of morbidity and mortality, especially in immunocompromised individuals. The innate immune system senses fungal pathogens through a family of Syk-coupled C-type lectin receptors (CLRs), which signal through the conserved immune adapter Card9. Although Card9 complexes are essential for antifungal defense in humans and mice, the mechanisms that couple CLR-proximal events to Card9 control are not well defined. Here, using a proteomic approach, we identified Vav proteins as key activators of the Card9 pathway. Vav1, Vav2 and Vav3 cooperate downstream of Dectin-1, Dectin-2 and Mincle to selectively engage Card9 for NF-κB control and proinflammatory gene transcription but are not involved in MAPK activation. Although Vav family members show functional redundancy, Vav1/2/3 triple-deficient cells are severely impaired for NF-κB and cytokine responses upon stimulation with CLR agonists or hyphae, and Vav1/2/3-/- mice phenocopy Card9-/- animals with extreme susceptibility to fungi and rapid mortality upon Candida albicans infection. In this context, Vav3 is the single most important Vav in mice, and a polymorphism in human VAV3 is associated with susceptibility to candidemia in patients. Our results reveal a molecular mechanism for CLR-mediated Card9 regulation that controls innate immunity to fungal infections.

2017-02-10 | GSE83736 | GEO

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