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Differentiation of gastric ECL cells is altered in CCK2 receptor-deficient mice

Chen, DA; Zhao, CM; Al-Haider, W; Håkanson, Rolf LU ; Rehfeld, JF and Kopin, AS (2002) In Gastroenterology 123(2). p.577-585
Abstract
Background & Aims: Gastrin stimulation of the type 2 cholecystokinin (CCK2) receptor results in ECL cell proliferation and histamine secretion. This report describes the effects of targeted disruption of the CCK2 receptor gene on ECL cell morphology and function. Methods: The ECL cells in the oxyntic mucosa of CCK2 receptor-deficient (knockout [KO]) vs. wild-type (WT) mice were investigated by immunocytochemical and biochemical approaches, as well as by electron microscopy. Results: Immunocytochemistry demonstrates similar numbers (cells per millimeter of horizontal length of mucosa) of pancreastatin- or vesicle monoamine transporter-2 (VMAT-2)-immunoreactive cells in WT mice and KO mice. However, only WT mice harbor... (More)
Background & Aims: Gastrin stimulation of the type 2 cholecystokinin (CCK2) receptor results in ECL cell proliferation and histamine secretion. This report describes the effects of targeted disruption of the CCK2 receptor gene on ECL cell morphology and function. Methods: The ECL cells in the oxyntic mucosa of CCK2 receptor-deficient (knockout [KO]) vs. wild-type (WT) mice were investigated by immunocytochemical and biochemical approaches, as well as by electron microscopy. Results: Immunocytochemistry demonstrates similar numbers (cells per millimeter of horizontal length of mucosa) of pancreastatin- or vesicle monoamine transporter-2 (VMAT-2)-immunoreactive cells in WT mice and KO mice. However, only WT mice harbor histamine-immunoreactive ECL cells. The mucosal histamine content in KO mice (likely originating from mast cells) is only a minute fraction of that present in WT animals. The activity of the histamine forming enzyme, histidine decarboxylase (a marker of ECL cells), was undetectable in the oxyntic mucosa of KO mice yet was readily apparent in the mucosa from WT animals. Electron microscopy revealed numerous ECL cells in WT mice. In KO animals, these cells were replaced by an "ECL-like" cell type, characterized by a lack of secretory vesicles (a hallmark feature of normal ECL cells) and the presence of dense-core granules and microvesicles in numbers comparable to those found in WT ECL cells. Based on ultrastructural features, the ECL-like cells in KO mice can be readily distinguished from other gastric endocrine cells, including A-like cells and D cells. Conclusions: Absence of a single gene product, the CCK2 receptor, alters the differentiation and function of gastric ECL cells. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Gastroenterology
volume
123
issue
2
pages
577 - 585
publisher
W B Saunders
external identifiers
  • wos:000177085400021
  • pmid:12145810
  • scopus:0036328972
ISSN
1528-0012
DOI
10.1053/gast.2002.34746
language
English
LU publication?
yes
id
f82a7d8f-ab38-4eb1-8665-9a38ec51ce38 (old id 332359)
date added to LUP
2007-08-14 14:51:49
date last changed
2017-06-04 03:33:25
@article{f82a7d8f-ab38-4eb1-8665-9a38ec51ce38,
  abstract     = {Background & Aims: Gastrin stimulation of the type 2 cholecystokinin (CCK2) receptor results in ECL cell proliferation and histamine secretion. This report describes the effects of targeted disruption of the CCK2 receptor gene on ECL cell morphology and function. Methods: The ECL cells in the oxyntic mucosa of CCK2 receptor-deficient (knockout [KO]) vs. wild-type (WT) mice were investigated by immunocytochemical and biochemical approaches, as well as by electron microscopy. Results: Immunocytochemistry demonstrates similar numbers (cells per millimeter of horizontal length of mucosa) of pancreastatin- or vesicle monoamine transporter-2 (VMAT-2)-immunoreactive cells in WT mice and KO mice. However, only WT mice harbor histamine-immunoreactive ECL cells. The mucosal histamine content in KO mice (likely originating from mast cells) is only a minute fraction of that present in WT animals. The activity of the histamine forming enzyme, histidine decarboxylase (a marker of ECL cells), was undetectable in the oxyntic mucosa of KO mice yet was readily apparent in the mucosa from WT animals. Electron microscopy revealed numerous ECL cells in WT mice. In KO animals, these cells were replaced by an "ECL-like" cell type, characterized by a lack of secretory vesicles (a hallmark feature of normal ECL cells) and the presence of dense-core granules and microvesicles in numbers comparable to those found in WT ECL cells. Based on ultrastructural features, the ECL-like cells in KO mice can be readily distinguished from other gastric endocrine cells, including A-like cells and D cells. Conclusions: Absence of a single gene product, the CCK2 receptor, alters the differentiation and function of gastric ECL cells.},
  author       = {Chen, DA and Zhao, CM and Al-Haider, W and Håkanson, Rolf and Rehfeld, JF and Kopin, AS},
  issn         = {1528-0012},
  language     = {eng},
  number       = {2},
  pages        = {577--585},
  publisher    = {W B Saunders},
  series       = {Gastroenterology},
  title        = {Differentiation of gastric ECL cells is altered in CCK2 receptor-deficient mice},
  url          = {http://dx.doi.org/10.1053/gast.2002.34746},
  volume       = {123},
  year         = {2002},
}