Functional VIP receptors in the human mucus-secreting colonic epithelial cell line CL.16E

Laburthe, Marc; Augeron, Chantal; Rouyer‐Fessard, Christiane; Roumagnac, I.; Maoret, Jean‐José; Grasset, E.; Laboisse, Christian L.

doi:10.1152/ajpgi.1989.256.3.g443

Cited by 36 publications

(30 citation statements)

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“…The duration of CCh or growth factor treatment has previously been shown by our group to be optimal for stimulation of EGFR phosphorylation in this system (12). In addition, the concentration of CCh used is physiologically relevant and is well established as the prototypic stimulus of GPCRinduced calcium-dependent chloride secretion across intestinal epithelial cells by our group and others (13,20,21). Western blot analysis of cell lysate supernatants immunoprecipitated with an anti-EGFR antibody and probed for phosphotyrosine showed that CCh and EGF induced EGFR phosphorylation as expected (Fig.…”

Section: Egf and Tgf-␣ Have Different Potencies In Stimulating Phosphmentioning

confidence: 75%

Consequences of Direct Versus Indirect Activation of Epidermal Growth Factor Receptor in Intestinal Epithelial Cells Are Dictated by Protein-tyrosine Phosphatase 1B

McCole

Truong

Bunz

et al. 2007

Journal of Biological Chemistry

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The epidermal growth factor receptor (EGFR) is an integral regulator of many cellular functions. EGFR also acts as a central conduit for extracellular signals involving direct activation of the receptor by EGFR ligands or indirect activation by G protein-coupled receptor (GPCR)-stimulated transactivation of the EGFR. We have previously shown that EGFR negatively regulates epithelial chloride secretion as a result of transforming growth factor-␣-mediated EGFR transactivation in response to muscarinic GPCR activation. Here we show that direct activation of the EGFR by EGFR ligands produces a different pattern of EGFR tyrosine phosphorylation and downstream phosphatidylinositol 3-kinase recruitment than GPCR-stimulated transactivation of the EGFR occurring via paracrine EGFR ligand release. Moreover, we demonstrate that this differential signaling and its consequences depend on protein-tyrosine phosphatase 1B activity. Thus protein-tyrosine phosphatase 1B governs differential recruitment of signaling pathways involved in EGFR regulation of epithelial ion transport. Our findings furthermore establish how divergent signaling outcomes can arise from the activation of a single receptor.All cell types rely on a limited set of receptors and signaling intermediates to translate extracellular information into appropriate acute and chronic changes in cellular behavior. Furthermore, many receptors mediate their effects via the secondary recruitment of other receptor types, including by stimulating the release of ligands for the downstream receptor (1, 2). A well studied example of this paradigm relates to cross-talk between G-protein-coupled receptors and a variety of receptor tyrosine kinases. In some cases this receptor-tyrosine kinase "transactivation" results in different downstream consequences than does direct activation of the receptor with its endogenous ligand (3, 4). However, a fundamental question remains as to how a single receptor, after activation by binding of either exogenous or endogenous ligand, can recruit distinct sets of downstream effectors and associated physiological outcomes. Epidermal growth factor receptor (EGFR)2 is one of four members of the ErbB receptor family, the other members being ErbB2, ErbB3, and ErbB4. Although ErbB2 has no known ligand of its own, it possesses the greatest enzymatic activity of the four isoforms and is the preferred dimerization partner for the other three receptors (5). The complexity of ErbB receptor activity is amplified by the large number of peptide ligands described for these receptors. All of these peptides originate as transmembrane precursors that are then enzymatically cleaved, thus releasing mature soluble ligands, including the EGFR ligands, EGF, and transforming growth factor ␣ (TGF-␣). The latter is the most abundant EGFR ligand found in the gastrointestinal tract (6, 7). After ligand binding, ErbB receptors undergo autophosphorylation and dimerization to form catalytically active homo-or heterodimers (8). The composition of these receptor dimers dictates ...

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Section: Egf and Tgf-␣ Have Different Potencies In Stimulating Phosphmentioning

confidence: 75%

Consequences of Direct Versus Indirect Activation of Epidermal Growth Factor Receptor in Intestinal Epithelial Cells Are Dictated by Protein-tyrosine Phosphatase 1B

McCole

Truong

Bunz

et al. 2007

Journal of Biological Chemistry

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“…This is a malignant human colon carcinoma cell line that differentiates, upon contact inhibition of cell growth, into normal-appearing polarized goblet cells that synthesize and secrete colonspecific mucin (Augeron and Laboisse, 1984;Augenlicht et al, 1987;Laburthe et al, 1989;Merlin et al, 1994). Since transition between these states seems to recapitulate the normal growth arrest and lineage-specific differentiation of colonic progenitor cells that is mediated by reduction of Notch signaling in the intestine (Yang et al, 2001;Shroyer et al, 2007), we focused on this cell line to investigate the potential role of Notch signaling in general, and Jagged1 specifically, in regulating Notch signaling in the colon carcinoma cell phenotype.…”

Section: Resultsmentioning

confidence: 99%

Heterogeneity of Jagged1 expression in human and mouse intestinal tumors: implications for targeting Notch signaling

et al. 2009

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“…Both secreted and membrane-bound intestinal mucins have been characterized in HT29-MTX and HT29-FU cell subpopulations, since MUC2 and MUC4 were highly expressed in HT29-FU and MUC3 and MUC5AC were highly expressed in HT29-MTX (62)(63)(64)(65)(66)(67)(68). The mucin-secreting HT-29 cell clones and subpopulations have been used to investigate the regulation of mucus transport (69)(70)(71)(72)(73)(74)(75)(76)(77)(78) and the functionality of human intestinal mucin-secreting cells (26,27). Moreover, mucin-secreting HT-29 cell subpopulations and clones have been used to investigate the role of human mucins in bacterial pathogenesis (62,63,(79)(80)(81).…”

Section: Differentiated Mucin-secreting Ht-29 Cell Subpopulations Andmentioning

confidence: 99%

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Moal

Servin

2013

Microbiol Mol Biol Rev

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SUMMARY Hosts are protected from attack by potentially harmful enteric microorganisms, viruses, and parasites by the polarized fully differentiated epithelial cells that make up the epithelium, providing a physical and functional barrier. Enterovirulent bacteria interact with the epithelial polarized cells lining the intestinal barrier, and some invade the cells. A better understanding of the cross talk between enterovirulent bacteria and the polarized intestinal cells has resulted in the identification of essential enterovirulent bacterial structures and virulence gene products playing pivotal roles in pathogenesis. Cultured animal cell lines and cultured human nonintestinal, undifferentiated epithelial cells have been extensively used for understanding the mechanisms by which some human enterovirulent bacteria induce intestinal disorders. Human colon carcinoma cell lines which are able to express in culture the functional and structural characteristics of mature enterocytes and goblet cells have been established, mimicking structurally and functionally an intestinal epithelial barrier. Moreover, Caco-2-derived M-like cells have been established, mimicking the bacterial capture property of M cells of Peyer's patches. This review intends to analyze the cellular and molecular mechanisms of pathogenesis of human enterovirulent bacteria observed in infected cultured human colon carcinoma enterocyte-like HT-29 subpopulations, enterocyte-like Caco-2 and clone cells, the colonic T84 cell line, HT-29 mucus-secreting cell subpopulations, and Caco-2-derived M-like cells, including cell association, cell entry, intracellular lifestyle, structural lesions at the brush border, functional lesions in enterocytes and goblet cells, functional and structural lesions at the junctional domain, and host cellular defense responses.

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Functional VIP receptors in the human mucus-secreting colonic epithelial cell line CL.16E

Cited by 36 publications

References 0 publications

Consequences of Direct Versus Indirect Activation of Epidermal Growth Factor Receptor in Intestinal Epithelial Cells Are Dictated by Protein-tyrosine Phosphatase 1B

Consequences of Direct Versus Indirect Activation of Epidermal Growth Factor Receptor in Intestinal Epithelial Cells Are Dictated by Protein-tyrosine Phosphatase 1B

Heterogeneity of Jagged1 expression in human and mouse intestinal tumors: implications for targeting Notch signaling

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

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