Regulation of gastrointestinal mucosal growth

Johnson, L. R.

doi:10.1152/physrev.1988.68.2.456

Cited by 279 publications

(163 citation statements)

References 0 publications

Supporting

Mentioning

155

Contrasting

Unclassified

Order By: Relevance

“…This binding was similarly inhibited by CCK-8, indicating that this receptor is shared by both gastrin and CCK. In contrast, G-Gly displaced the specific binding only at 10 Ϫ6 M. Thus gastrin upregulated the expression of its own receptor in GSM06 cells (14). …”

Section: Resultsmentioning

confidence: 84%

“…We initially failed to detect specific [ 125 I]gastrin binding to the membrane fraction of GSM06 cells. Because Johnson (14) and Takeuchi et al (40) reported that gastrin stimulation increases the expression of its own receptor, we precultured the cells with 10 Ϫ7 M gastrin for 48 h, then performed an [ 125 I]gastrin binding study. With this gastrin pretreatment, we detected specific binding of [ 125 I]gastrin on GSM06 cell membranes, which was competitively inhibited by an increase in exogenous gastrin and CCK-8.…”

Section: Discussionmentioning

confidence: 99%

“…Thus these findings suggest that gastrin directly stimulates the growth of the pit cell lineage by inducing its own receptor in pit cell precursors. gastric mucosal growth; gastric surface mucous cell; gastrin/ cholecystokinin-B receptor GASTRIN CONTROLS THE GROWTH of gastric mucosa (14,15). Hypertrophied gastric mucosa is observed in patients with gastrin-producing tumors and also in rats infused continuously with gastrin (5, 31).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Gastrin stimulates the growth of gastric pit cell precursors by inducing its own receptors

Nakajima

Konda

Izumi

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

.-Gastrin/CCK-B receptors (CCKB-Rs) are present on parietal and enterochromaffin-like cells in the gastric mucosa but not on pit cells in the proliferative zone. Because serum gastrin levels are well correlated with the growth of the gastric pit, we examined whether pit precursor cells express CCKB-Rs using hypergastrinemic transgenic mice and a mouse pit precursor cell line, GSM06. In situ hybridization indicated that CCKB-R mRNA was limited to the lower one-third of the mucosa in control mice, whereas it was faintly distributed along the midto low glandular region in the hypergastrinemic transgenic mouse mucosa. CCKB-R-positive midglandular cells appear to have a pit cell lineage; therefore, GSM06 cells were used for an [ 125 I]gastrin binding study. [ 125 I]gastrin bound to the membrane fraction of the GSM06 cells when precultured with gastrin. Gastrin dose dependently induced CCKB-R expression in GSM06 cells and stimulated their growth. Thus these findings suggest that gastrin directly stimulates the growth of the pit cell lineage by inducing its own receptor in pit cell precursors. gastric mucosal growth; gastric surface mucous cell; gastrin/ cholecystokinin-B receptor GASTRIN CONTROLS THE GROWTH of gastric mucosa (14,15). Hypertrophied gastric mucosa is observed in patients with gastrin-producing tumors and also in rats infused continuously with gastrin (5, 31). In contrast, hypotrophic or atrophic mucosa results from fasting in rats whose serum gastrin levels become low (35). The glandular cell components, which include parietal, chief, and enterochromaffin-like (ECL) cells, have relatively long lifespans of 3, 5, and 2 mo, respectively (17). Thus the atrophic change induced by fasting in rats appears to be due mainly to a shortage of pit/gastric surface mucous cells that survive only 3 days in rodents (18). It is not known, however, whether the pit cells and their precursors express gastrin receptors.The physiological roles of gastrin in mucosal growth were recently studied using hypergastrinemic animal models. Wang et al. (45) produced transgenic (TG) mice expressing gastrin under the control of an insulin promoter, which resulted in gastrin production in pancreatic ␤-cells. They reported that gastrin enhances gastric mucosal growth, whereas progastrin preferentially stimulates colonic mucosal growth. They further demonstrated that hypergastrinemic TG mice develop gastric atrophy and eventually gastric cancer (44) and postulated that the hyperplasia of the foveolar pit cell region and the decrease in the parietal cell mass are due, at least in part, to gastrin-stimulated upregulation of growth factors, including heparin binding-epidermal growth factor-like growth factor (HB-EGF) and transforming growth factor-␣ (TGF-␣). Moreover, infection with Helicobacter felis accelerates the formation of gastric cancer in a synergistic manner with hypergastrinemia in hypergastrinemic TG mice (44).We generated TG mice with hypergastrinemia by expressing a human gastrin transgene (19). The gastric mucosa of these mice...

show abstract

Section: Resultsmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Gastrin stimulates the growth of gastric pit cell precursors by inducing its own receptors

Nakajima

Konda

Izumi

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

show abstract

“…For mammals, luminal, secretory, hormonal, and neural signals have each been implicated to stimulate intestinal response, including mucosal growth (Gershon et al, 1994;Johnson and McCormack, 1994;Solomon, 1994;Walsh, 1994). For the Burmese python, it has been demonstrated that the sight and smell of food, the stretching of their stomach using a balloon catheter, the luminal presence of pancreaticobiliary secretions, and the intestinal infusion of saline and glucose solution each fail to generate a morphological response by the intestine (Secor, et al, 2002).…”

Section: Enterocyte Hypertrophymentioning

confidence: 99%

Postprandial morphological response of the intestinal epithelium of the Burmese python (Python molurus)

Lignot

Helmstetter

Secor

2005

Comparative Biochemistry and Physiology Part A: Molecular &

106

View full text Add to dashboard Cite

The postprandial morphological changes of the intestinal epithelium of Burmese pythons were examined using fasting pythons and at eight time points after feeding. In fasting pythons, tightly packed enterocytes possess very short microvilli and are arranged in a pseudostratified fashion.Enterocyte width increases by 23% within 24 h postfeeding, inducing significant increases in villus length and intestinal mass. By 6 days postfeeding, enterocyte volume had peaked, following as much as an 80% increase. Contributing to enterocyte hypertrophy is the cellular accumulation of lipid droplets at the tips and edges of the villi of the proximal and middle small intestine, but were absent in the distal small intestine. At 3 days postfeeding, conventional and environmental scanning electron microscopy revealed cracks and lipid extrusion along the narrow edges of the villi and at the villus tips. Transmission electron microscopy demonstrated the rapid postprandial lengthening of enterocyte microvilli, increasing 4.8-fold in length within 24 h, and the maintaining of that length through digestion. Beginning at 24 h postfeeding, spherical particles were found embedded apically within enterocytes of the proximal and middle small intestine. These particles possessed an annular-like construction and were stained with the calcium-stain Alizarine red S suggesting that they were bone in origin. Following the completion of digestion, many of the postprandial responses were reversed, as observed by the atrophy of enterocytes, the shortening of villi, and the retraction of the microvilli. Further exploration of the python intestine will reveal the underlying mechanisms of these trophic responses and the origin and fate of the engulfed particles.

show abstract

“…The mammalian intestinal epithelium is a rapidly self-renewing tissue in the body, and its homeostasis is preserved through strict regulation of epithelial cell proliferation, growth arrest, and apoptosis (1)(2)(3). Under physiological conditions, the epithelium of the human small intestine undergoes ϳ10 11 mitoses per day (4).…”

mentioning

confidence: 99%

Polyamine Depletion Increases Cytoplasmic Levels of RNA-binding Protein HuR Leading to Stabilization of Nucleophosmin and p53 mRNAs

Zou¹,

Mazan-Mamczarz

Rao³

et al. 2006

Journal of Biological Chemistry

114

167

View full text Add to dashboard Cite

Polyamines are essential for maintaining normal intestinal epithelial integrity, an effect that relies, at least in part, on their ability to keep low levels of nucleophosmin (NPM) and p53 mRNAs. The RNA-binding protein HuR associates with the p53 mRNA, as reported previously, and with the NPM mRNA, computationally predicted to be a target of HuR. Here, we show that HuR binds the NPM and p53 3-untranslated regions and stabilizes these mRNAs in polyaminedepleted intestinal epithelial cells. Depletion of cellular polyamines by inhibiting ornithine decarboxylase with ␣-difluoromethylornithine dramatically enhanced the cytoplasmic abundance of HuR, whereas ectopic ornithine decarboxylase overexpression decreased cytoplasmic HuR; neither intervention changed whole-cell HuR levels. HuR was found to specifically bind the 3-untranslated regions of NPN and p53 mRNAs. HuR silencing rendered the NPM and p53 mRNAs unstable and prevented increases in NPM and p53 mRNA and protein in polyamine-deficient cells. These results indicate that polyamines modulate cytoplasmic HuR levels in intestinal epithelial cells, in turn controlling the stability of the NPM and p53 mRNAs and influencing NPM and p53 protein levels.

show abstract

Regulation of gastrointestinal mucosal growth

Cited by 279 publications

References 0 publications

Gastrin stimulates the growth of gastric pit cell precursors by inducing its own receptors

Gastrin stimulates the growth of gastric pit cell precursors by inducing its own receptors

Postprandial morphological response of the intestinal epithelium of the Burmese python (Python molurus)

Polyamine Depletion Increases Cytoplasmic Levels of RNA-binding Protein HuR Leading to Stabilization of Nucleophosmin and p53 mRNAs

Contact Info

Product

Resources

About