Origin, differentiation and renewal of the four main epithelial cell types in the mouse small intestine II. Mucous cells

1974 ◽  
Vol 141 (4) ◽  
pp. 481-501 ◽  
Author(s):  
Hazel Cheng
Keyword(s):  
Small Intestine ◽  
Epithelial Cell ◽  
Cell Types ◽  
Mucous Cells ◽  
Mouse Small Intestine

Regulation of gene expression in gastric epithelial cell populations of fetal, neonatal, and adult transgenic mice

1992 ◽  
Vol 263 (2) ◽  
pp. G186-G197 ◽  
Author(s):  
K. A. Roth ◽  
S. M. Cohn ◽  
D. C. Rubin ◽  
J. F. Trahair ◽  
M. R. Neutra ◽  
...  
Keyword(s):  
Gene Expression ◽  
Small Intestine ◽  
Epithelial Cell ◽  
Regulation Of Gene Expression ◽  
Cell Types ◽  
Gastric Epithelium ◽  
Single Type ◽  
Cell Populations ◽  
Mucous Cells ◽  
Fabp Gene

Little is known about lineage relationships and differentiation programs of various epithelial cells present in mouse gastric units. We have previously used rat liver fatty acid binding protein/human growth hormone (L-FABP/hGH) transgenes to define epithelial cell lineages relationships in the small intestine of fetal and adult mice and to examine regulation of their terminal differentiation programs along the crypt-to-villus and duodenal-to-ileal axes. We have now used these transgenes to explore similar issues in the stomach. Immunocytochemical studies of fetal and adult transgenic L-FABP/hGH animals and their normal littermates revealed that the intact endogenous mouse L-FABP gene (Fabpl) is not expressed in gastric epithelium. Nucleotides-596 to +21 of the rat L-FABP gene direct "inappropriate" expression of hGH in the gastric epithelium as early as fetal day 15. From 1 to 13 mo, L-FABP-596 to +21/hGH expression occurs only in surface mucous cells of zymogenic and mucous gastric units; the reporter is not detectable in the enteroendocrine, parietal and chief cell populations of zymogenic glands. Electron microscopic immunocytochemistry revealed that hGH is directed to apical secretory granules in surface and pit mucous cells expressing the transgene. hGH levels vary widely among surface mucous cells both within single pits and between gastric units in a given animal. The heterogeneity noted in reporter expression suggests that there are marked differences in the regulatory environments of individual cells of a single type within a given gastric unit. This raises the possibility that cell differentiation programs in the stomach may not be as tightly coupled to cellular translocation as in the small intestine. Finally, the lack of expression of L-FABP-596 to +21/hGH in gastrin- and serotonin-immunoreactive cells of the stomach contrasts with its efficient expression in comparable cell types located in the duodenum; providing a model system for examining differential regulation of gene expression in terminally differentiated cell types represented in both gastric and intestinal epithelium.

scholarly journals Intestinal renewal across the animal kingdom: comparing stem cell activity in mouse and Drosophila

2019 ◽  
Vol 316 (3) ◽  
pp. G313-G322 ◽  
Author(s):  
Rachel K. Zwick ◽  
Benjamin Ohlstein ◽  
Ophir D. Klein
Keyword(s):  
Small Intestine ◽  
Therapeutic Potential ◽  
Cell Activity ◽  
Cell Types ◽  
Intestinal Stem Cells ◽  
Gi Tract ◽  
Mouse Small Intestine ◽  
Stem Cell Activity ◽  
Cellular Source ◽  
The Face

The gastrointestinal (GI) tract renews frequently to sustain nutrient digestion and absorption in the face of consistent tissue stress. In many species, proliferative intestinal stem cells (ISCs) are responsible for the repair of the damage arising from chemical and mechanical aspects of food breakdown and exposure to pathogens. As the cellular source of all mature cell types of the intestinal epithelium throughout adulthood, ISCs hold tremendous therapeutic potential for understanding and treating GI disease in humans. This review focuses on recent advances in our understanding of ISC identity, behavior, and regulation during homeostasis and injury-induced repair, as revealed by two major animal models used to study regeneration of the small intestine: Drosophila melanogaster and Mus musculus. We emphasize recent findings from Drosophila that are likely to translate to the mammalian GI system, as well as challenging topics in mouse ISC biology that may be ideally suited for investigation in flies. For context, we begin by reviewing major physiological similarities and distinctions between the Drosophila midgut and mouse small intestine.

scholarly journals Fibroblast growth factor 10 alters the balance between goblet and Paneth cells in the adult mouse small intestine

2015 ◽  
Vol 308 (8) ◽  
pp. G678-G690 ◽  
Author(s):  
Denise Al Alam ◽  
Soula Danopoulos ◽  
Kathy Schall ◽  
Frederic G. Sala ◽  
Dana Almohazey ◽  
...  
Keyword(s):  
Small Intestine ◽  
Cell Differentiation ◽  
Epithelial Cell ◽  
Paneth Cells ◽  
Intestinal Epithelial ◽  
Mouse Small Intestine ◽  
Fibroblast Growth Factor 10 ◽  
Goblet Cell Differentiation

Intestinal epithelial cell renewal relies on the right balance of epithelial cell migration, proliferation, differentiation, and apoptosis. Intestinal epithelial cells consist of absorptive and secretory lineage. The latter is comprised of goblet, Paneth, and enteroendocrine cells. Fibroblast growth factor 10 (FGF10) plays a central role in epithelial cell proliferation, survival, and differentiation in several organs. The expression pattern of FGF10 and its receptors in both human and mouse intestine and their role in small intestine have yet to be investigated. First, we analyzed the expression of FGF10, FGFR1, and FGFR2, in the human ileum and throughout the adult mouse small intestine. We found that FGF10, FGFR1b, and FGFR2b are expressed in the human ileum as well as in the mouse small intestine. We then used transgenic mouse models to overexpress Fgf10 and a soluble form of Fgfr2b, to study the impact of gain or loss of Fgf signaling in the adult small intestine. We demonstrated that overexpression of Fgf10 in vivo and in vitro induces goblet cell differentiation while decreasing Paneth cells. Moreover, FGF10 decreases stem cell markers such as Lgr5, Lrig1, Hopx, Ascl2, and Sox9. FGF10 inhibited Hes1 expression in vitro, suggesting that FGF10 induces goblet cell differentiation likely through the inhibition of Notch signaling. Interestingly, Fgf10 overexpression for 3 days in vivo and in vitro increased the number of Mmp7/Muc2 double-positive cells, suggesting that goblet cells replace Paneth cells. Further studies are needed to determine the mechanism by which Fgf10 alters cell differentiation in the small intestine.

scholarly journals NHERF3 is necessary for Escherichia coli heat-stable enterotoxin-induced inhibition of NHE3: differences in signaling in mouse small intestine and Caco-2 cells

2019 ◽  
Vol 317 (4) ◽  
pp. C737-C748
Author(s):  
Tiane Chen ◽  
Ruxian Lin ◽  
Leela Avula ◽  
Rafiquel Sarker ◽  
Jianbo Yang ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Small Intestine ◽  
Intracellular Signaling ◽  
Cell Types ◽  
Enterotoxigenic Escherichia Coli ◽  
Intracellular Cgmp ◽  
Heat Stable ◽  
Mouse Small Intestine ◽  
Intracellular Ca ◽  
Multiple Cell

Enterotoxigenic Escherichia coli (ETEC) is a leading cause of childhood death from diarrhea and the leading cause of Traveler’s diarrhea. E. coli heat-stable enterotoxin (ST) is a major virulence factor of ETEC and inhibits the brush border Na/H exchanger NHE3 in producing diarrhea. NHE3 regulation involves multiprotein signaling complexes that form on its COOH terminus. In this study, the hypothesis was tested that ST signals via members of the Na/H exchanger regulatory factor (NHERF) family of scaffolding proteins, NHERF2, which had been previously shown to have a role, and now with concentration on a role for NHERF3. Two models were used: mouse small intestine and Caco-2/BBe cells. In both models, ST rapidly increased intracellular cGMP, inhibited NHE3 activity, and caused a quantitatively similar decrease in apical expression of NHE3. The transport effects were NHERF3 and NHERF2 dependent. Also, mutation of the COOH-terminal amino acids of NHERF3 supported that NHERF3-NHERF2 heterodimerization was likely to account for this dual dependence. The ST increase in cGMP in both models was partially dependent on NHERF3. The intracellular signaling pathways by which ST-cGMP inhibits NHE3 were different in mouse jejunum (activation of cGMP kinase II, cGKII) and Caco-2 cells, which do not express cGKII (elevation of intracellular Ca2+ concentration [Ca2+]i). The ST elevation of [Ca2+]i was from intracellular stores and was dependent on NHERF3-NHERF2. This study shows that intracellular signaling in the same diarrheal model in multiple cell types may be different; this has implications for therapeutic strategies, which often assume that models have similar signaling mechanisms.

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