Comparative analysis of neutral endopeptidase (NEP) and villin gene expression during mouse embryogenesis and enterocyte maturation

Landry, Claire; Huet, Christian; Mangeat, Paul; Sahuquet, Alain; Louvard, Daniel; Crine, Philippe

doi:10.1046/j.1432-0436.1994.56120055.x

Cited by 11 publications

(6 citation statements)

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“…3A ). We detected PEDV infection in differentiated mature enterocyte cells that express villin, which serves as a surface marker for differentiated intestinal epithelial cells and is expressed in cells located in the brush border of the intestine ( 25 , 26 ). Moreover, we observed PEDV infection (nucleocapsid positive) in Lgr5 + stem cells, Ki-67-positive (proliferating) cells, and Muc2 + goblet cells, although the number of PEDV-positive cells in the latter two cell populations was limited ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Porcine Intestinal Enteroids: a New Model for Studying Enteric Coronavirus Porcine Epidemic Diarrhea Virus Infection and the Host Innate Response

Guo

et al. 2019

J Virol

106

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Porcine epidemic diarrhea virus (PEDV), a member of the group of alphacoronaviruses, is the pathogen of a highly contagious gastrointestinal swine disease. The elucidation of the events associated with the intestinal epithelial response to PEDV infection has been limited by the absence of good in vitro porcine intestinal models that recapitulate the multicellular complexity of the gastrointestinal tract. Here, we generated swine enteroids from the intestinal crypt stem cells of the duodenum, jejunum, or ileum and found that the generated enteroids are able to satisfactorily recapitulate the complicated intestinal epithelium in vivo and are susceptible to infection by PEDV. PEDV infected multiple types of cells, including enterocytes, stem cells, and goblet cells, and exhibited segmental infection discrepancies compared with ileal enteroids and colonoids, and this finding was verified in vivo. Moreover, the clinical isolate PEDV-JMS propagated better in ileal enteroids than the cell-adapted isolate PEDV-CV777, and PEDV infection suppressed interferon (IFN) production early during the infection course. IFN lambda elicited a potent antiviral response and inhibited PEDV in enteroids more efficiently than IFN alpha (IFN-␣). Therefore, swine enteroids provide a novel in vitro model for exploring the pathogenesis of PEDV and for the in vitro study of the interplay between a host and a variety of swine enteric viruses. IMPORTANCE PEDV is a highly contagious enteric coronavirus that causes significant economic losses, and the lack of a good in vitro model system is a major roadblock to an in-depth understanding of PEDV pathogenesis. Here, we generated a porcine intestinal enteroid model for PEDV infection. Utilizing porcine intestinal enteroids, we demonstrated that PEDV infects multiple lineages of the intestinal epithelium and preferably infects ileal enteroids over colonoids and that enteroids prefer to respond to IFN lambda 1 over IFN-␣. These events recapitulate the events that occur in vivo. This study constitutes the first use of a primary intestinal enteroid model to investigate the susceptibility of porcine enteroids to PEDV and to determine the antiviral response following infection. Our study provides important insights into the events associated with PEDV infection of the porcine intestine and provides a valuable in vitro model for studying not only PEDV but also other swine enteric viruses.

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Section: Resultsmentioning

confidence: 99%

Porcine Intestinal Enteroids: a New Model for Studying Enteric Coronavirus Porcine Epidemic Diarrhea Virus Infection and the Host Innate Response

Guo

et al. 2019

J Virol

106

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“…Although there are some limitations inherent in trying to use immunoperoxidase histochemistry as a quantitative measure, our results suggest that maximal small espin accumulation occurs not early, but relatively late during enterocyte differentiation and brush border assembly. In contrast, both villin and fimbrin/plastin have been found to be nearly as prevalent in the apical cytoplasm of crypt cells in the adult as they are in the brush borders of the mature enterocytes ( Fath et al, 1990 ; Heintzelman and Mooseker, 1990 ; Landry et al, 1994 ). The increase in immunoperoxidase staining for small espin was first noted for enterocytes nearing the crypt–villus junction, roughly coinciding with the timing of the terminal elongation of microvilli and the arrival of brush border myosin I ( Heintzelman and Mooseker, 1992 ; Fath and Burgess, 1995 ).…”

Section: Discussionmentioning

confidence: 99%

Small Espin: A Third Actin-bundling Protein and Potential Forked Protein Ortholog in Brush Border Microvilli

Bartles

Zheng

et al. 1998

The Journal of Cell Biology

143

208

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An ∼30-kD isoform of the actin-binding/ bundling protein espin has been discovered in the brush borders of absorptive epithelial cells in rat intestine and kidney. Small espin is identical in sequence to the COOH terminus of the larger (∼110-kD) espin isoform identified in the actin bundles of Sertoli cell–spermatid junctional plaques (Bartles, J.R., A. Wierda, and L. Zheng. 1996. J. Cell Sci. 109:1229–1239), but it contains two unique peptides at its NH2 terminus. Small espin was localized to the parallel actin bundles of brush border microvilli, resisted extraction with Triton X-100, and accumulated in the brush border during enterocyte differentiation/migration along the crypt–villus axis in adults. In transfected BHK fibroblasts, green fluorescent protein–small espin decorated F-actin–containing fibers and appeared to elicit their accumulation and/or bundling. Recombinant small espin bound to skeletal muscle and nonmuscle F-actin with high affinity (K d = 150 and 50 nM) and cross-linked the filaments into bundles. Sedimentation, gel filtration, and circular dichroism analyses suggested that recombinant small espin was a monomer with an asymmetrical shape and a high percentage of α-helix. Deletion mutagenesis suggested that small espin contained two actin-binding sites in its COOH-terminal 116–amino acid peptide and that the NH2-terminal half of its forked homology peptide was necessary for bundling activity.

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“…Their expressions might be differentially regulated by the restricted MUC5AC presence on surface epithelial cells (Reis et al 1997), MUC6 on cells in the glandular compartment of pyloric mucosa (Ho et al 1995;Reis et al 2000), and MUC2 in the goblet cells of small and large intestines, and on IM (Jass 2000). A secreting endopeptidase, CD10 (Landry et al 1994;Sezaki et al 2003), and one of the actin-binding cytoskeletal proteins, villin (Landry et al 1994;MacLennan et al 1999;Pinto et al 1999), are also observed in intestinal cells, whose expressions indicate absorptivecell differentiation in IM (Landry et al 1994). Expressions of these molecules are widely used to evaluate gastric cancers whether the differentiation direction is toward gastric or intestinal phenotype.…”

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confidence: 99%

Mixed Gastric- and Intestinal-type Metaplasia Is Formed by Cells with Dual Intestinal and Gastric Differentiation

Niwa

Ikehara

Nakanishi

et al. 2005

J Histochem Cytochem.

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We have proposed to divide intestinal metaplasia (IM) into two categories, i.e., a mixed gastric and intestinal (GI) type, and a solely intestinal (I) type, based on the residual gastric phenotype cells. The GI-mixed-type IM can be identified by the presence of both cells with either gastric or intestinal phenotypes in a single gland. This study is conducted to elucidate whether cells in the GI-mixed-type IM glands can simultaneously present both gastric and intestinal phenotypes. MUC5AC, MUC2, CD10 and villin expressions were investigated in 20 samples from five gastric cancer cases, directly using either AlexaFluor 488- or 568-labeled specific monoclonal antibodies and observed by fluorescent microscopy and confocal laser-scanning microscopy. GI-mixed IM glands comprise a population expressing MUC5AC and MUC2, MUC5AC and villin, and MUC5AC and CD10. MUC2 and villin expressions were reciprocally increased with decreasing MUC5AC expression, while CD10 expression was limited to cells with only a residual MUC5AC expression or no expression. These results suggest that a heterogeneous cell population with both gastric and intestinal phenotypes would develop into a single intestinal phenotype, as reflected in the progression of intestinal metaplasia from GI-mixed-type- to I-type IM-type glands.

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Comparative analysis of neutral endopeptidase (NEP) and villin gene expression during mouse embryogenesis and enterocyte maturation

Cited by 11 publications

References 54 publications

Porcine Intestinal Enteroids: a New Model for Studying Enteric Coronavirus Porcine Epidemic Diarrhea Virus Infection and the Host Innate Response

Porcine Intestinal Enteroids: a New Model for Studying Enteric Coronavirus Porcine Epidemic Diarrhea Virus Infection and the Host Innate Response

Small Espin: A Third Actin-bundling Protein and Potential Forked Protein Ortholog in Brush Border Microvilli

Mixed Gastric- and Intestinal-type Metaplasia Is Formed by Cells with Dual Intestinal and Gastric Differentiation

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