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Gastric phenotypic abnormality in cholecystokinin 2 receptor null mice

Chen, D; Zhao, CM; Håkanson, Rolf LU and Rehfeld, JF (2002) In Pharmacology and Toxicology1987-01-01+01:002004-01-01+01:00 91(6). p.375-381
Abstract
Gastrin, released from antral G-cells, plays an important role in the regulation of gastric acid secretion and is trophic for the stomach, The cholecystokinin type 2 (CCK)(2) receptor (previously referred to as CCK-B/gastrin receptors) is expressed in both parietal cells and ECL cells in the oxyntic mucosa of stomach. Gastric phenotypic abnormality has been observed in CCK2 receptor null (gene knock-out) mice. Such mice displayed markedly impaired gastric acid secretion, atrophy of the oxyntic mucosa and hypergastrinaemia. The impaired acid secretion may be the result of a reduced parietal cell mass, a reduced proportion of actively secreting parietal cells (with secretory canaliculi), and a replacement of ECL cells by histamine-free... (More)
Gastrin, released from antral G-cells, plays an important role in the regulation of gastric acid secretion and is trophic for the stomach, The cholecystokinin type 2 (CCK)(2) receptor (previously referred to as CCK-B/gastrin receptors) is expressed in both parietal cells and ECL cells in the oxyntic mucosa of stomach. Gastric phenotypic abnormality has been observed in CCK2 receptor null (gene knock-out) mice. Such mice displayed markedly impaired gastric acid secretion, atrophy of the oxyntic mucosa and hypergastrinaemia. The impaired acid secretion may be the result of a reduced parietal cell mass, a reduced proportion of actively secreting parietal cells (with secretory canaliculi), and a replacement of ECL cells by histamine-free ECL-like cells. The ECL-like cells, observed in the CCK2 receptor null mice, lacked the hallmark features of wild-type ECL cells, i.e. histamine and cytoplasmic secretory vesicles. However, they had the features of endocrine cells, such as the content of pancreastatin (a fragment of chromogranin A), with cytoplasmic small dense-core granules and microvesicles. We propose that the replacement of ECL cells by ECL-like cells in the mutant mice reflects an altered differentiation of the same precursors that develop into ECL cells in wild-type mice. Thus, studies of CCK2 receptor null mice demonstrate the importance of the receptor in the regulation of gastric acid secretion and in the differentiation of ECL cells in the oxyntic mucosa of stomach. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Pharmacology and Toxicology1987-01-01+01:002004-01-01+01:00
volume
91
issue
6
pages
375 - 381
publisher
Wiley-Blackwell
external identifiers
  • wos:000180230200015
  • pmid:12688382
  • scopus:0036970217
ISSN
1600-0773
DOI
10.1034/j.1600-0773.2002.910616.x
language
English
LU publication?
yes
id
b2a59de3-2503-4ed5-abf7-72b7f4103e41 (old id 320213)
date added to LUP
2007-08-14 14:49:46
date last changed
2017-11-27 13:09:29
@article{b2a59de3-2503-4ed5-abf7-72b7f4103e41,
  abstract     = {Gastrin, released from antral G-cells, plays an important role in the regulation of gastric acid secretion and is trophic for the stomach, The cholecystokinin type 2 (CCK)(2) receptor (previously referred to as CCK-B/gastrin receptors) is expressed in both parietal cells and ECL cells in the oxyntic mucosa of stomach. Gastric phenotypic abnormality has been observed in CCK2 receptor null (gene knock-out) mice. Such mice displayed markedly impaired gastric acid secretion, atrophy of the oxyntic mucosa and hypergastrinaemia. The impaired acid secretion may be the result of a reduced parietal cell mass, a reduced proportion of actively secreting parietal cells (with secretory canaliculi), and a replacement of ECL cells by histamine-free ECL-like cells. The ECL-like cells, observed in the CCK2 receptor null mice, lacked the hallmark features of wild-type ECL cells, i.e. histamine and cytoplasmic secretory vesicles. However, they had the features of endocrine cells, such as the content of pancreastatin (a fragment of chromogranin A), with cytoplasmic small dense-core granules and microvesicles. We propose that the replacement of ECL cells by ECL-like cells in the mutant mice reflects an altered differentiation of the same precursors that develop into ECL cells in wild-type mice. Thus, studies of CCK2 receptor null mice demonstrate the importance of the receptor in the regulation of gastric acid secretion and in the differentiation of ECL cells in the oxyntic mucosa of stomach.},
  author       = {Chen, D and Zhao, CM and Håkanson, Rolf and Rehfeld, JF},
  issn         = {1600-0773},
  language     = {eng},
  number       = {6},
  pages        = {375--381},
  publisher    = {Wiley-Blackwell},
  series       = {Pharmacology and Toxicology1987-01-01+01:002004-01-01+01:00},
  title        = {Gastric phenotypic abnormality in cholecystokinin 2 receptor null mice},
  url          = {http://dx.doi.org/10.1034/j.1600-0773.2002.910616.x},
  volume       = {91},
  year         = {2002},
}