Academic literature on the topic 'Mouse intestinal epithelium'
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Journal articles on the topic "Mouse intestinal epithelium"
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Darmoul, D., D. Brown, M. E. Selsted, and A. J. Ouellette. "Cryptdin gene expression in developing mouse small intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 1 (January 1, 1997): G197—G206. http://dx.doi.org/10.1152/ajpgi.1997.272.1.g197.
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In rodents, the four intestinal epithelial cell lineages differentiate and become morphologically distinct during the first 2-3 postnatal wk. In studies reported here, reverse transcriptase-polymerase chain reaction (RT-PCR)-based assays detected Paneth cell defensin mRNAs in intestinal RNA from 1-day-old (P1) mice before crypt formation and maturation of the epithelium. Analysis of these defensin-coding RT-PCR products from P1 mice showed that 69% of clones sequenced coded for cryptdin-6, suggesting that it is the most abundant enteric defensin mRNA in the newborn. Paneth cell mRNAs, including cryptdins-4 and -5, lysozyme, matrilysin, and defensin-related sequences, also were detected in RNA from P1 mouse intestine. Unlike adult mice, where only Paneth cells are immunopositive for cryptdin, cryptdin-containing cells were distributed throughout the newborn intestinal epithelium and not in association with rudimentary crypts. Cryptdin immunoreactivity in the P1 mouse intestine was specific for intracellular granule contents, and immunofluorescent detection of cryptdins on mucosal surfaces suggested that the peptides are released into the intestinal lumen in P1 mice Defensin secretion may contribute to innate immunity of the neonatal intestine before the presence of distinguishable Paneth cells.
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Schjoldager, Katrine T. B. G., Henrik R. Maltesen, Sophie Balmer, Leif R. Lund, Mogens H. Claesson, Hans Sjöström, Jesper T. Troelsen, and Jørgen Olsen. "Cellular cross talk in the small intestinal mucosa: postnatal lymphocytic immigration elicits a specific epithelial transcriptional response." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 6 (June 2008): G1335—G1343. http://dx.doi.org/10.1152/ajpgi.00265.2007.
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During the early postnatal period lymphocytes migrate into the mouse small intestine. Migrating infiltrative lymphocytes have the potential to affect the epithelial cells via secreted cytokines. Such cross talk can result in the elicitation of an epithelial transcriptional response. Knowledge about such physiological cross talk between the immune system and the epithelium in the postnatal small intestinal mucosa is lacking. We have investigated the transcriptome changes occurring in the postnatal mouse small intestine using DNA microarray technology, immunocytochemistry, and quantitative real-time RT-PCR analysis. The DNA microarray data were analyzed bioinformatically by using a combination of projections to latent structures analysis and functional annotation analysis. The results show that infiltrating lymphocytes appear in the mouse small intestine in the late postweaning period and give rise to distinct changes in the epithelial transcriptome. Of particular interest is the expression of three genes encoding a mucin ( Muc4), a mucinlike protein ( 16000D21Rik), and ATP citrate lyase (Acly). All three genes were shown to be expressed by the epithelium and to be upregulated in response to lymphocytic migration into the small intestinal mucosa.
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Hofmann, Felix, Torsten Thalheim, Karen Rother, Marianne Quaas, Christiane Kerner, Jens Przybilla, Gabriela Aust, and Joerg Galle. "How to Obtain a Mega-Intestine with Normal Morphology: In Silico Modelling of Postnatal Intestinal Growth in a Cd97-Transgenic Mouse." International Journal of Molecular Sciences 22, no. 14 (July 8, 2021): 7345. http://dx.doi.org/10.3390/ijms22147345.
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Intestinal cylindrical growth peaks in mice a few weeks after birth, simultaneously with crypt fission activity. It nearly stops after weaning and cannot be reactivated later. Transgenic mice expressing Cd97/Adgre5 in the intestinal epithelium develop a mega-intestine with normal microscopic morphology in adult mice. Here, we demonstrate premature intestinal differentiation in Cd97/Adgre5 transgenic mice at both the cellular and molecular levels until postnatal day 14. Subsequently, the growth of the intestinal epithelium becomes activated and its maturation suppressed. These changes are paralleled by postnatal regulation of growth factors and by an increased expression of secretory cell markers, suggesting growth activation of non-epithelial tissue layers as the origin of enforced tissue growth. To understand postnatal intestinal growth mechanistically, we study epithelial fate decisions during this period with the use of a 3D individual cell-based computer model. In the model, the expansion of the intestinal stem cell (SC) population, a prerequisite for crypt fission, is largely independent of the tissue growth rate and is therefore not spontaneously adaptive. Accordingly, the model suggests that, besides the growth activation of non-epithelial tissue layers, the formation of a mega-intestine requires a released growth control in the epithelium, enabling accelerated SC expansion. The similar intestinal morphology in Cd97/Adgre5 transgenic and wild type mice indicates a synchronization of tissue growth and SC expansion, likely by a crypt density-controlled contact inhibition of growth of intestinal SC proliferation. The formation of a mega-intestine with normal microscopic morphology turns out to originate in changes of autonomous and conditional specification of the intestinal cell fate induced by the activation of Cd97/Adgre5.
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Chen, Chin, Rixun Fang, Corrine Davis, Charalambos Maravelias, and Eric Sibley. "Pdx1 inactivation restricted to the intestinal epithelium in mice alters duodenal gene expression in enterocytes and enteroendocrine cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 6 (December 2009): G1126—G1137. http://dx.doi.org/10.1152/ajpgi.90586.2008.
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Null mutant mice lacking the transcription factor pancreatic and duodenal homeobox 1 (Pdx1) are apancreatic and survive only a few days after birth. The role of Pdx1 in regulating intestinal gene expression has therefore yet to be determined in viable mice with normal pancreatic development. We hypothesized that conditional inactivation of Pdx1 restricted to the intestinal epithelium would alter intestinal gene expression and cell differentiation. Pdx1 flox/flox; VilCre mice with intestine-specific Pdx1 inactivation were generated by crossing a transgenic mouse strain expressing Cre recombinase, driven by a mouse villin 1 gene promoter fragment, with a mutant mouse strain homozygous for loxP site-flanked Pdx1. Pdx1 protein is undetectable in all epithelial cells in the intestinal epithelium of Pdx1 flox/flox; VilCre mice. Goblet cell number and mRNA abundance for mucin 3 and mucin 13 genes in the proximal small intestine are comparable between Pdx1 flox/flox; VilCre and control mice. Similarly, Paneth cell number and expression of Paneth cell-related genes Defa1, Defcr-rs1, and Mmp7 in the proximal small intestine remain statistically unchanged by Pdx1 inactivation. Although the number of enteroendocrine cells expressing chromogranin A/B, gastric inhibitory polypeptide (Gip), or somatostatin (Sst) is unaffected in the Pdx1 flox/flox; VilCre mice, mRNA abundance for Gip and Sst is significantly reduced in the proximal small intestine. Conditional Pdx1 inactivation attenuates intestinal alkaline phosphatase (IAP) activity in the duodenal epithelium, consistent with an average 91% decrease in expression of the mouse enterocyte IAP gene, alkaline phosphatase 3 (a novel Pdx1 target candidate), in the proximal small intestine following Pdx1 inactivation. We conclude that Pdx1 is necessary for patterning appropriate gene expression in enterocytes and enteroendocrine cells of the proximal small intestine.
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Maharshak, Nitsan, Eun Young Huh, Chorlada Paiboonrungruang, Michael Shanahan, Lance Thurlow, Jeremy Herzog, Zorka Djukic, et al. "Enterococcus faecalis Gelatinase Mediates Intestinal Permeability via Protease-Activated Receptor 2." Infection and Immunity 83, no. 7 (April 27, 2015): 2762–70. http://dx.doi.org/10.1128/iai.00425-15.
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Microbial protease-mediated disruption of the intestinal epithelium is a potential mechanism whereby a dysbiotic enteric microbiota can lead to disease. This mechanism was investigated using the colitogenic, protease-secreting enteric microbeEnterococcus faecalis. Caco-2 and T-84 epithelial cell monolayers and the mouse colonic epithelium were exposed to concentrated conditioned media (CCM) fromE. faecalisV583 andE. faecalislacking the gelatinase gene (gelE). The flux of fluorescein isothiocyanate (FITC)-labeled dextran across monolayers or the mouse epithelium following exposure to CCM from parental or mutantE. faecalisstrains indicated paracellular permeability. A protease-activated receptor 2 (PAR2) antagonist and PAR2-deficient (PAR2−/−) mice were used to investigate the role of this receptor inE. faecalis-induced permeability. Gelatinase (GelE) purified fromE. faecalisV583 was used to confirm the ability of this protease to induce epithelial cell permeability and activate PAR2. The protease-mediated permeability of colonic epithelia from wild-type (WT) and PAR2−/−mice by fecal supernatants from ulcerative colitis patients was assessed. SecretedE. faecalisproteins induced permeability in epithelial cell monolayers, which was reduced in the absence ofgelEor by blocking PAR2 activity. SecretedE. faecalisproteins induced permeability in the colonic epithelia of WT mice that was absent in tissues from PAR2−/−mice. Purified GelE confirmed the ability of this protease to induce epithelial cell permeability via PAR2 activation. Fecal supernatants from ulcerative colitis patients induced permeability in the colonic epithelia of WT mice that was reduced in tissues from PAR2−/−mice. Our investigations demonstrate that GelE fromE. faecaliscan regulate enteric epithelial permeability via PAR2.
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Babeu, Jean-Philippe, Mathieu Darsigny, Carine R. Lussier, and François Boudreau. "Hepatocyte nuclear factor 4α contributes to an intestinal epithelial phenotype in vitro and plays a partial role in mouse intestinal epithelium differentiation." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 1 (July 2009): G124—G134. http://dx.doi.org/10.1152/ajpgi.90690.2008.
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Hepatocyte nuclear factor 4α (HNF4α) is a regulator of hepatocyte and pancreatic transcription. Hnf4α deletion in the mouse is embryonically lethal with severe defects in visceral endoderm formation. It has been concluded in the past that the role of Hnf4α in the developing colon was much less important than in the liver. However, the precise role of Hnf4α in the homeostasis of the small intestinal epithelium remains unclear. Our aim was to evaluate the potential of Hnf4α to support an intestinal epithelial phenotype. First, Hnf4α potential to dictate this phenotype was assessed in nonintestinal cell lines in vitro. Forced expression of Hnf4α in fibroblasts showed an induction of features normally restricted to epithelial cells. Combinatory expression of Hnf4α with specific transcriptional regulators of the intestine resulted in the induction of intestinal epithelial genes in this context. Second, the importance of Hnf4α in maintaining the homeostasis of the intestinal epithelium was investigated in mice. Mice conditionally deficient for intestinal Hnf4α developed normally throughout adulthood with an epithelium displaying normal morphological and functional structures with minor alterations. Subtle but statistical differences were observed at the proliferation and the cytodifferentiation levels. Hnf4α mutant mice displayed an increase in the number of goblet and enteroendocrine cells compared with controls. Given the fundamental role of this transcription factor in other tissues, these findings dispute the crucial role for this regulator in the maintenance of intestinal epithelial cell function at a period of time that follows cytodifferentiation but may suggest a functional role in instructing cells to become specific to the intestinal epithelium.
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Li, Yan, Yun-Yan Xiang, Wei-Yang Lu, Chuanyong Liu, and Jingxin Li. "A novel role of intestine epithelial GABAergic signaling in regulating intestinal fluid secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 4 (August 15, 2012): G453—G460. http://dx.doi.org/10.1152/ajpgi.00497.2011.
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γ-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous system, and it is produced via the enzymatic activity of glutamic acid decarboxylase (GAD). GABA generates fast biological signaling through type A receptors (GABAAR), an anionic channel. Intriguingly, GABA is found in the jejunum epithelium of rats. The present study intended to determine whether a functional GABA signaling system exists in the intestinal epithelium and if so whether the GABA signaling regulates intestinal epithelial functions. RT-PCR, Western blot, and immunohistochemical assays of small intestinal tissues of various species were performed to determine the expression of GABA-signaling proteins in intestinal epithelial cells. Perforated patch-clamp recording was used to measure GABA-induced transmembrane current in the small intestine epithelial cell line IEC-18. The fluid weight-to-intestine length ratio was measured in mice that were treated with GABAAR agonist and antagonist. The effect of GABAAR antagonist on allergic diarrhea was examined using a mouse model. GABA, GAD, and GABAAR subunits were identified in small intestine epithelial cells of mice, rats, pigs, and humans. GABAAR agonist induced an inward current and depolarized IEC-18. Both GABA and the GABAAR agonist muscimol increased intestinal fluid secretion of rats. The increased intestinal secretion was largely decreased by the GABAAR antagonist picrotoxin or gabazine, but not by tetrodotoxin. The expression levels of GABA-signaling proteins were increased in the intestinal epithelium of mice that were sensitized and challenged with ovalbumin (OVA). The OVA-treated mice exhibited diarrhea, which was alleviated by oral administration of gabazine or picrotoxin. An endogenous autocrine GABAergic signaling exists in the mammalian intestinal epithelium, which upregulates intestinal fluid secretion. The intestinal GABAergic signaling becomes intensified in allergic diarrhea, and inhibition of this GABA-signal system alleviates the allergic diarrhea.
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Gerbe, François, Johan H. van Es, Leila Makrini, Bénédicte Brulin, Georg Mellitzer, Sylvie Robine, Béatrice Romagnolo, et al. "Distinct ATOH1 and Neurog3 requirements define tuft cells as a new secretory cell type in the intestinal epithelium." Journal of Cell Biology 192, no. 5 (March 7, 2011): 767–80. http://dx.doi.org/10.1083/jcb.201010127.
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The unique morphology of tuft cells was first revealed by electron microscopy analyses in several endoderm-derived epithelia. Here, we explore the relationship of these cells with the other cell types of the intestinal epithelium and describe the first marker signature allowing their unambiguous identification. We demonstrate that although mature tuft cells express DCLK1, a putative marker of quiescent stem cells, they are post-mitotic, short lived, derive from Lgr5-expressing epithelial stem cells, and are found in mouse and human tumors. We show that whereas the ATOH1/MATH1 transcription factor is essential for their differentiation, Neurog3, SOX9, GFI1, and SPDEF are dispensable, which distinguishes these cells from enteroendocrine, Paneth, and goblet cells, and raises from three to four the number of secretory cell types in the intestinal epithelium. Moreover, we show that tuft cells are the main source of endogenous intestinal opioids and are the only epithelial cells that express cyclooxygenase enzymes, suggesting important roles for these cells in the intestinal epithelium physiopathology.
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Blache, Philippe, Marc van de Wetering, Isabelle Duluc, Claire Domon, Philippe Berta, Jean-Noël Freund, Hans Clevers, and Philippe Jay. "SOX9 is an intestine crypt transcription factor, is regulated by the Wnt pathway, and represses the CDX2 and MUC2 genes." Journal of Cell Biology 166, no. 1 (July 5, 2004): 37–47. http://dx.doi.org/10.1083/jcb.200311021.
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TCF and SOX proteins belong to the high mobility group box transcription factor family. Whereas TCFs, the transcriptional effectors of the Wnt pathway, have been widely implicated in the development, homeostasis and disease of the intestine epithelium, little is known about the function of the SOX proteins in this tissue. Here, we identified SOX9 in a SOX expression screening in the mouse fetal intestine. We report that the SOX9 protein is expressed in the intestinal epithelium in a pattern characteristic of Wnt targets. We provide in vitro and in vivo evidence that a bipartite β-catenin/TCF4 transcription factor, the effector of the Wnt signaling pathway, is required for SOX9 expression in epithelial cells. Finally, in colon epithelium-derived cells, SOX9 transcriptionally represses the CDX2 and MUC2 genes, normally expressed in the mature villus cells of the intestinal epithelium, and may therefore contribute to the Wnt-dependent maintenance of a progenitor cell phenotype.
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Hodges, Craig A., Brian R. Grady, Kirtishri Mishra, Calvin U. Cotton, and Mitchell L. Drumm. "Cystic fibrosis growth retardation is not correlated with loss of Cftr in the intestinal epithelium." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 3 (September 2011): G528—G536. http://dx.doi.org/10.1152/ajpgi.00052.2011.
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Maldigestion due to exocrine pancreatic insufficiency leads to intestinal malabsorption and consequent malnutrition, a mechanism proposed to cause growth retardation associated with cystic fibrosis (CF). However, although enzyme replacement therapy combined with increased caloric intake improves weight gain, the effect on stature is not significant, suggesting that growth retardation has a more complex etiology. Mouse models of CF support this, since these animals do not experience exocrine pancreatic insufficiency yet are growth impaired. Cftr absence from the intestinal epithelium has been suggested as a primary source of growth retardation in CF mice, a concept we directly tested by generating mouse models with Cftr selectively inactivated or restored in intestinal epithelium. The relationship between growth and functional characteristics of the intestines, including transepithelial electrophysiology, incidence of intestinal obstruction, and histopathology, were assessed. Absence of Cftr exclusively from intestinal epithelium resulted in loss of cAMP-stimulated short-circuit current, goblet cell hyperplasia, and occurrence of intestinal obstructions but only slight and transient impaired growth. In contrast, specifically restoring Cftr to the intestinal epithelium resulted in restoration of ion transport and completely protected against obstruction and histopathological anomalies, but growth was indistinguishable from CF mice. These results indicate that absence of Cftr in the intestinal epithelium is an important contributor to the intestinal obstruction phenotype in CF but does not correlate with the observed growth reduction in CF.
Dissertations / Theses on the topic "Mouse intestinal epithelium"
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Kelly, Shane. "Proteomic analysis of APC deficient mouse intestinal epithelium." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609442.
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Quinlan, Jonathan Mark. "In vitro culture of embryonic mouse intestinal epithelium and adenoviral-mediated gene delivery." Thesis, University of Bath, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501614.
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Study of the normal development of the intestinal epithelium has been hampered by a lack of suitable model systems, in particular ones that enable the introduction of exogenous genes. Production of such a system would advance our understanding of normal epithelial development and help to shed light on the pathogenesis of intestinal neoplasia. The criteria for a reliable culture system include the ability to perform real time observations and manipulations in vitro, the preparation of wholemounts for immunostaining and the potential for introducing genes.
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O'Sullivan, John F. "Cell lineage analysis of the liver and the intestinal epithelium of the mouse." Thesis, University of Reading, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.276221.
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Cambuli, Francesca Maria. "Study of Musashi1-Expressing cells and of Musashi1 function in mouse intestinal physiopathology." Thesis, Lyon, École normale supérieure, 2012. http://www.theses.fr/2012ENSL0794.
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L’épithélium intestinal est une monocouche de cellules qui tapisse la lumière intestinale, constitué d’un compartiment différencié, les villosités dans l’intestin grêle et les plateaux épithéliaux dans le colon, et d’un compartiment prolifératif, les cryptes de Lieberkühn. Ce tissue se renouvelle de façon rapide et continue tout au long de la vie de l’individu, grâce à la présence de cellules souches adultes dans le fond des cryptes. Ces cellules s’autorenouvellent et donnent naissance à des progéniteurs prolifératifs (capables d’engendrer les différents cytotypes épithéliaux) qui se différencient tout en migrant vers le compartiment différencié. Mon travail de these a porté sur l’étude d’une marqueur putatif de ces cellules souches épithéliales intestinales: Musashi1 (Msi1).Dans ce contexte, mon premier axe d’étude s’est focalisé sur l’isolement et la caractérisation des cellules souches épithéliales intestinales chez la souris. Pour cela, nous avons généré des souris transgéniques exprimant la protéine fluorescente GFP sous le contrôle du promoteur de Msi1. Les cellules souches intestinales de ces souris coexpriment donc Msi1 et la GFP. Ce modèle a été validé et nous à permis de isoler les cellules GFP/Msi1 positives dans l’intestin. A l'aide de différentes approches cellulaires et moléculaires, nous avons confirmé leur nature de cellules souches et nous avons apporté des nouvelles données sur la composition de la zone proliférative de l’épithélium intestinal murin.Le second axe de mes travaux de thèse a porté sur l’étude de la fonction de Msi1 dans l'homéostasie de l’épithélium intestinal chez la souris, par son sur-expression tous au long de l’épithélium. Nous avons montré que la sur-expression de cette protéine, qui est un régulateur des voies Wnt et Notch, perturbe l’architecture intestinale, a propriétés pro-prolifératives et un potentiel tumorigèniqueThe intestinal epithelium is a monolayer of cells surrounding the intestinal lumen. It consists of a differentiated compartment, the villi in the small intestine and a flat surface in the colon, and a proliferative compartment, the crypts of Lieberkühn. This tissue self-renews rapidly and continuously throughout life, due to the presence of adult stem cells in the bottom of the crypts. These cells are capable of self-renewing and give rise to proliferating progenitors (capable of generating all the different epithelial cytotypes) that differentiate and migrate toward the differentiated compartment. My thesis focused on the study of the intestinal epithelial stem cells marker Musashi1 (Msi1).In this context, the first part of my thesis work focused on the isolation and characterization of the intestinal epithelial stem cells that express Msi1 in the mouse. For this, we generated transgenic mice expressing the fluorescent protein GFP under the control of the promoter of Msi1. The intestinal stem cells of these mice co-express Msi1 and GFP. This model has been validated and allowed us to isolate GFP+/Msi-expressing cells in the intestine. By using different cellular and molecular approches, we confirmed their nature of stem cells and provided new data on the composition of the proliferative zone in the murine intestinal epithelium.The second part of my thesis has focused on the study of the function of Msi1 in the intestinal epithelium homeostasis in the mouse, by its over- and ectopic expression all along the epithelium. We have shown that the over-expression of this protein, which is a regulator of the Wnt and Notch pathways, perturbs the intestinal architecture, has pro-proliferative properties and tumorigenic potential
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Slaymi, Chaker. "Rôle de la GTPase atypique RhoU dans l'homéostasie intestinale." Thesis, Montpellier 2, 2014. http://www.theses.fr/2014MON20127.
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L'épithélium intestinal se renouvelle tous les 4 à 6 jours chez les mammifères grâce aux cellules souches localisées au fond des cryptes. Le renouvellement dépend des signaux émis par le microenvironnement et requiert une phase de prolifération des cellules souches, de différenciation et d'apoptose/desquamation des cellules épithéliales. La signalisation Wnt, joue un rôle majeur dans l'homéostasie intestinale par l'action de deux gradients inversés le long de l'axe crypte/lumière ; la signalisation Wnt canonique, active au fond des cryptes, contrôle la prolifération alors que la signalisation non-canonique, active vers le haut des cryptes contrôle la différenciation. Il a été montré que ces deux voies contrôlent l'activité de la GTPase atypique RhoU/Wrch1. RhoU fait partie des GTPases qui s'activent spontanément, son activité est donc directement proportionnelle à son niveau d'expression dans la cellule. Enfin, cette GTPase atypique est sous exprimée dans de nombreuses tumeurs gastriques et colorectales.Compte tenu de ces données, nos objectifs étaient donc de caractériser les changements morphologiques induits par l'invalidation conditionnelle de RhoU dans l'épithélium intestinal murin et d'en déterminer les mécanismes d'action. Nos résultats montrent que la déplétion de RhoU n'est pas létale, cependant elle a induit une augmentation de 20% de la densité cellulaire et une désorganisation de la structure de l'épithélium dans le haut des cryptes du colon. Cette augmentation concerne aussi bien les lignages sécrétoires et absorptifs, cependant, l'absence de RhoU a induit une sur-représentation du lignage sécrétoire. Dans la lignée de tumeur colorectale DLD-1, nous avons montré que l'absence de RhoU mime le phénotype d'augmentation de la densité cellulaire observé chez la souris. L'invalidation de RhoU ne modifie pas la distribution des phases du cycle cellulaire ni de celle de la mitose, cependant, elle réduit le nombre des cellules en apoptose dans le colon des souris et dans les cellules DLD-1. L'invalidation de RhoU a réduit la signalisation Hippo et a altéré la contractilité cellulaire via une augmentation de la phosphorylation de la protéine MLC2. Des travaux récents ont montré que la diminution du niveau MLC2 phosphorylée est nécessaire pour l'activation des caspases par un stimulus apoptotique. Ceci suggère que cette perturbation de la contractilité peut être à l'origine de cette diminution de l'apoptose qui est la cause majeure responsable de ce phénotype. En conclusion, RhoU est un régulateur de l'homéostasie intestinale chez la souris via son rôle modérateur de la mort cellulaireIn Mammals, the intestinal epithelium is renewed every 4-6 days through the stem cells located at the bottom of crypts. The renewal depends on signals from the micro-environment and requires a proliferation phase of stem cells, then a differentiation and apoptosis/desquamation phases of epithelial cells. Wnt signaling plays a major role in intestinal homeostasis by the action of two reversed gradients along the axis crypt/ lumen: canonical Wnt signaling, active in the bottom of crypts, control proliferation while non canonical signaling, active in the top of the crypts control cell differentiation. It was shown that these two pathways are regulator of the atypical GTPase RhoU/Wrch1. The RhoU protein activates spontaneously, its activity is directly proportional to its expression level in the cell and is expressed as in gastric and colorectal tumors. In view of these informations, our objectives were therefore to characterizethe morphological changes induced by conditional invalidation of RhoU in the intestinal epithelium of mice and to determine the mechanisms of action. Our results show that RhoU depletion is not lethal. However, it induces an increase of cell density (+20%) and a disruption of the epithelium structure in the top of the colonic crypts. This increase affects both absorptive and secretory lineages. However, the absence of RhoU induced over-representation of secretory lineage. In colorectal tumor cell line DLD-1, we have shown that the absence of RhoU mimics the phenotype of cell density increase observed in mice. RhoU invalidationdid not change the distribution of cell cycle phases and mitosis, however, it reduces the number of apoptotic cells in the colon of mice and in the DLD-1 cells. RhoU invalidation reduced Hippo signaling and altered cell contractility via the increase of the protein MLC2 phosphorylation. Recent work has shown that the reduction of MLC2-P level is necessary for the caspase protein activation by an apoptotic stimulus. Suggesting that the perturbation of contractility may be the cause of this apoptosis decrease which is the main cause responsible of this phenotype. Finally, RhoU is a regulator of the intestinal homeostasis in micevia its moderating role of cell death
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Berger, Emanuel [Verfasser]. "Impact of unfolded protein responses on intestinal epithelial homeostasis in genetically modified mouse models / Emanuel Berger." München : Verlag Dr. Hut, 2014. http://d-nb.info/1055863680/34.
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Berger, Emanuel Clemens [Verfasser]. "Impact of unfolded protein responses on intestinal epithelial homeostasis in genetically modified mouse models / Emanuel Berger." München : Verlag Dr. Hut, 2014. http://nbn-resolving.de/urn:nbn:de:101:1-2014081529049.
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Singh, J. C. I., S. M. Cruickshank, D. J. Newton, L. Wakenshaw, Anne M. Graham, J. Lan, J. P. A. Lodge, P. J. Felsburg, and S. R. Carding. "Toll-like receptor-mediated responses of primary intestinal epithelial cells during the development of colitis." The American Physiological Society, 2004. http://hdl.handle.net/10454/4048.
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noThe interleukin-2-deficient (IL-2¿/¿) mouse model of ulcerative colitis was used to test the hypothesis that colonic epithelial cells (CEC) directly respond to bacterial antigens and that alterations in Toll-like receptor (TLR)-mediated signaling may occur during the development of colitis. TLR expression and activation of TLR-mediated signaling pathways in primary CEC of healthy animals was compared with CEC in IL-2¿/¿ mice during the development of colitis. In healthy animals, CEC expressed functional TLR, and in response to the TLR4 ligand LPS, proliferated and secreted the cytokines IL-6 and monocyte chemoattractant protein-1 (MCP-1). However, the TLR-responsiveness of CEC in IL-2¿/¿ mice was different with decreased TLR4 responsiveness and augmented TLR2 responses that result in IL-6 and MCP-1 secretion. TLR signaling in CEC did not involve NF-B (p65) activation with the inhibitory p50 form of NF-B predominating in CEC in both the healthy and inflamed colon. Development of colitis was, however, associated with the activation of MAPK family members and upregulation of MyD88-independent signaling pathways characterized by increased caspase-1 activity and IL-18 production. These findings identify changes in TLR expression and signaling during the development of colitis that may contribute to changes in the host response to bacterial antigens seen in colitis.
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Tirelle, Pauline. "Role du microbiote intestinal dans la régulation de l'axe intestin-cerveau au cours du modèle murin d'anorexie " activity-based anorexia Gut microbiota alteration in a mouse model of Anorexia Nervosa Comparison of different modes of antibiotic delivery on gut microbiota depletion efficiency and body composition in mouse Gut microbiota depletion affects nutritional and bahavioral responses to activity-based anorexia model in a sex-dependent manner Invalidation of Toll-like receptor 4 in intestinal epithelial cells modifies the response to activity base anorexia model in a sex-dependent manner." Thesis, Normandie, 2020. http://www.theses.fr/2020NORMR056.
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L’anorexie mentale (AN) est un trouble du comportement alimentaire (TCA) à prédominance féminine, principalement caractérisée par une diminution de l’apport alimentaire entrainant une forte perte de poids. Par ailleurs, de nombreuses comorbidités sont retrouvées à l’image de la dépression et de l’anxiété. Ces dernières années, l’étude du rôle de l’axe microbiote-intestin-cerveau dans les TCA ainsi que l’anxiété a gagné en intérêt. Ainsi, des études ont rapporté une dysbiose du microbiote intestinal chez les patients anorexiques. Cependant la physiopathologie de l’AN demeure à l’heure actuelle encore mal comprise. Le but des travaux menés au cours de cette thèse, a été d’étudier le rôle du microbiote dans l’axe intestin-cerveau, au cours du modèle murin d’anorexie, activity-based anorexia (ABA) combinant activité physique spontanée et diminution progressive du temps d’accès à l’alimentation. La première étude réalisée au cours de ce projet, a eu pour objectif de caractériser le microbiote intestinal de souris C57Bl/6 mâles soumises au modèle ABA. Une augmentation des Lactobacilles et de clostridium cocleatum appartenant au genre Clostridium, ainsi qu’une diminution de Burkholderiales ont été observé chez les animaux ABA. Par ailleurs, de nombreuses corrélations entre différents groupes bactériens et la prise alimentaire, le poids corporel ainsi que la composition corporelle ont été soulignées. Afin d’étudier le rôle de la présence du microbiote intestinal au cours du modèle ABA, nous avons, lors d’un deuxième travail, mis en place un protocole de déplétion par antibiothérapie. Pour cela nous avons comparé différents modes d’administration d’une solution d’antibiotiques à large spectre, par gavage oral une ou deux fois par jour ou par administration dans l’eau de boisson. Bien que ces trois modes provoque une très forte diminution des bactéries présentent au niveau fécal, l’administration une fois par jour induit une prolifération des Gammaprotéobactéries. Par conséquent, l’administration par eau de boisson ou gavage oral deux fois par jours apparaissent comme les procédures les mieux adaptées pour dépléter le microbiote intestinal. Lors de la troisième étude effectuée au cours de cette thèse, nous avons étudié la réponse au modèle ABA chez des souris C57Bl/6 mâles et femelles dont le microbiote intestinal a été déplété par antibiothérapie. Tout d’abord il a été montré que l’administration d’antibiotiques, induisait une augmentation de la masse grasse et une diminution de la masse maigre. Suite au modèle ABA les animaux déplétés présentaient une plus faible diminution de leur poids corporel. Ce phénomène était d’autant plus marqué chez les mâles, chez lesquels un comportement anxieux a également été souligné. Cette étude a donc permis de montrer une réponse sexe-dépendante à la déplétion du microbiote intestinal au cours du modèle ABAAnorexia nervosa (AN) is an eating disorder (ED) with female predominance, mainly characterised by a decrease of food intake leading to a severe body weight loss. Furthermore, psychiatric comorbidities are frequently observed in AN patients such as depression and anxiety. During the last decade, the role of microbiota-gut-brain axis in ED and anxiety-like behavior has emerged. Several studies reported gut microbiota dysbiosis in anorectic patients. Nevertheless, the pathophysiology of AN remains poorly understood. The aim of the present PhD thesis was to better understand the contribution of the gut microbiota in the regulation of gut-brain axis in the mouse model of anorexia "activity-based anorexia" (ABA). The ABA model combines spontaneous physical activity with a free running wheel access and a progressive limited food access. In a first study, we characterised the gut microbiota of C57Bl/6 male mice submitted to ABA model. We observed in ABA mice an increase of Lactobacillus and clostridium cocleatum belonging to genus of Clostridium, as well as a decrease of Burkholderiales. Interestingly, correlations between bacteria taxa and food intake, body weight and body composition have been observed. Then, we aimed to evaluate the response to ABA model of mice with gut microbial depletion. We thus compared in a second study different dosing and administration of large spectrum antibiotic treatments, either by oral gavages (once or twice a day) or by addition in drinking water. Although these three strategies led to a strong decrease of faecal bacteria, once day oral gavage induced proliferation of Gammaproteobacteria. Thus, antibiotics administration by oral gavage twice a day or in drinking water appear as the most appropriate modes to achieve gut microbiota depletion. In a third study, we then evaluated the response to ABA model of both male and female C57Bl/6 mice with antibiotic-induced microbiota depletion. Firstly, we observed that antibiotic administration led to an increase of fat mass and a decrease of lean mass. During the ABA model, gut microbiota-depleted mice exhibited a lower decrease of body weight compared to untreated ABA mice. In males, we also observed altered anxiety-like behavior in ABA mice with depleted gut microbiota. We thus showed that gut microbiota-depleted mice exhibited an altered response to ABA model in a sex-dependent manner. Finally, in order to decipher the underlying mechanisms, we focused on toll-like receptor 4 (TLR4), an endogenous receptor of lipopolysaccharides. Previous studies suggested TLR4 implication in the regulation of feeding and anxiety-like behaviors. To determine the involvement of intestinal TLR4, we submitted mice with intestinal epithelial TLR4 knockout to the ABA model. Again, we observed a sex-dependent response: a delayed and limited body weight loss in males and an increase of anxiety-like behavior in females. In conclusion, studies performed during this PhD thesis highlight the alterations and the role of gut microbiota in the activity-based anorexia model that appear to be sex-dependent
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Schelp, Nadine. "Analysis of genetic interactions and hierarchies of Wnt-signaling components in vivo." Doctoral thesis, 2012. http://hdl.handle.net/11858/00-1735-0000-000D-FB61-E.
Full textAbstract:
Der Wnt/β-catenin Signalweg reguliert zusammen mit anderen Signalkaskaden die Embryogenese sowie auch die Homöostase und die Proliferation der Stammzellen im adulten Organismus. Mutationen in Komponenten dieses Signaltransduktionsweges führen zu einer aberranten Aktivierung von β-catenin und wurden in vielen verschieden Krebsarten einschließlich Darmkrebs beobachtet. Die transkriptionelle Akivität von β-catenin wird von verschiedenen nukleären Kofaktoren beeinflusst. Hierzu zählen insbesondere die Proteine der Pygopus Familie, die in Drosophila eine essentielle Rolle im kanonischen Wnt-Signalweg spielen, in Vertebraten allerdings vielmehr Kontext abhängig agieren. Insbesondere Pygo2 ist hierbei vermutlich auch an der malignen Transformation verschiedener Zelltypen mit anschließender Ausbildung von Tumoren beteiligt. Auch wenn bereits gezeigt werden konnte, dass Pygo2 in Darmtumoren überexprimiert wird, ist bisher unbekannt, ob es tatsächlich eine Rolle bei der Entstehung von intestinalen Tumoren spielt.
Anhand von genetischen Experimenten in der Maus zeigt diese Arbeit zum ersten Mal in vivo, dass Pygo2 für die normale Homöostase des Darms nicht essentiell ist, aber an der Ausbildung von Darmtumoren, welche durch eine Stabilisierung von β-catenin induziert werden, beteiligt ist. Weder im embryonalen noch im adulten Darm beeinflusste der konditionale Villin-Cre bedingte Knock-out von Pygo2 in epithelialen Zellen die normale embryonale Entwicklung oder die Homöostase im adulten Darm. Auch für die Regulation von Zielgenen des Wnt/β-catenin Signalweges unter physiologischen Bedingungen scheint Pygo2 funktionell redundant zu sein. Im Gegensatz dazu verhinderte der Verlust von Pygo2 die Entstehung von β-catenin induzierten intestinalen Tumoren und normalisierte die damit verbundene Hyperproliferation sowie die erhöhte Expression von Wnt/β-catenin Zielgenen und intestinalen Stammzellmarkern. Überraschenderweise konnte die Ausbildungen von Adenomen in ApcMin/+ Mäusen durch Deletion von Pygo2 nicht verhindert werden.
Der Vergleich beider Mausmodelle ergab eine erhöhte Expression von BCL9-2 in den Adenomen der ApcMin/+ Mäuse aber nicht in den Hyperplasien, die durch aktiviertes β-catenin induziert wurden. Dies könnte darauf hinweisen, dass in Apc mutierten epithelialen Zellen BCL9-2 für die Tumorprogression verantwortlich ist. Weiterhin konnte gezeigt werden, dass sowohl der knock-down von Pygo2 als auch von BCL9-2 in human Kolonkarzinomzellen die Proliferation reduzierte.
Anhand von immunohistochemischen Analysen des Phosphorylierungsstatus von ERK1/2, einem „downstream“ Effektor von K-ras, konnten außerdem pERK1/2 positive Zellen in den intestinalen Adenomen von ApcMin/+ Mäusen, nicht aber in hyperproliferierenden Zellen mit stabilisierten β-catenin nachgewiesen werden.
Zusammenfassend weisen die Ergebnisse dieser Arbeit daraufhin, dass die Funktion von Pygo2 im Darm Kontext abhängig ist. Während in normalen epithelialen Zellen des Darms Pygo2 offensichtlich funktionell redundant ist, scheint es für die Ausbildung von intestinalen Tumoren, welche durch dereguliertes Wnt/β-catenin induziert werden, essentiell zu sein. Daher könnte Pygo2 ein idealer Angriffspunkt für die zielgerichtete Therapie von Darmtumoren mit β-catenin Mutation sein.
Book chapters on the topic "Mouse intestinal epithelium"
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Sato, Toshiro, and Hans Clevers. "Primary Mouse Small Intestinal Epithelial Cell Cultures." In Methods in Molecular Biology, 319–28. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-125-7_19.
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Shaked, Helena, Monica Guma, and Michael Karin. "Analysis of NF-κB Activation in Mouse Intestinal Epithelial Cells." In Methods in Molecular Biology, 593–606. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2422-6_35.
Full textConference papers on the topic "Mouse intestinal epithelium"
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Nerurkar, Nandan L., and Cliff J. Tabin. "Collective Cell Movements Drive Morphogenesis and Elongation of the Avian Hindgut." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14438.
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At the end of gastrulation, the endoderm forms a single-cell thick epithelium lining the ventral surface of the developing embryo. Subsequently, through a series of poorly understood events, the initially flat endoderm is transformed into the gut tube, a cylindrical structure that gives rise to the epithelial lining of the entire respiratory and gastrointestinal tracts. In birds and mammals, formation of the gut tube begins with two invaginations at the anterior (head) and posterior (tail) poles of the embryo, termed the anterior (AIP) and caudal intestinal portals (CIP). It is thought that the AIP and CIP begin moving toward one another as two progressing waves of lateral-to medial folding (from left and right toward center), “zipping” the gut tube closed along the embryonic midline (Fig. 1A). This view of lateral-to-medial folding is, however, inconsistent with several observations. For example, fate mapping studies in chick and mouse that suggest that cells originating in the posterior end (toward the tail) of the flat endoderm do not form the hindgut, but instead contribute to the more anterior midgut [1, 2]. This would not be possible in a simple lateral-to-medial folding process. Therefore, it is largely unknown how this fundamental structure of the vertebrate body plan is established. The objective of the present work is to apply multi-photon live imaging of the chick embryo to determine how the hindgut is formed. Our findings suggest the hindgut arises from directed, collective cell movements that drive antero-posterior folding of the initially flat endoderm.
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Suman, Shubhankar, Santosh Kumar, Albert J. Fornace, and Kamal Datta. "Abstract 5465: Persistent oxidative stress in mouse intestinal and colonic epithelial cells after exposure to12C-ion radiation." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5465.
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Kim, Jong-Sang, Ji-Sun Lim, Annalene Garcia, Ji-Yeon Seo, Jia Park, Dae Hwan Nam, Mi Kyung Sung, and Young-Rok Seo. "Abstract 4579: Effect of pre-adipocyte and differentiated adipocyte conditioned media on galectin-3 expression in mouse intestinal epithelial cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4579.
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