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Antral G-cell in gastrin and gastrin-cholecystokinin knockout animals

Friis-Hansen, L; Wierup, Nils LU ; Rehfeld, J F and Sundler, Frank LU (2005) In Cell and Tissue Research 321(1). p.141-146
Abstract
The antral hormone gastrin is the key regulator of gastric acid secretion, mucosal growth and differentiation. Gastrin is synthesized in the endocrine G-cells in the antroduodenal mucosa. We have now examined the way in which the loss of gastrin alone or gastrin plus cholecystokinin (CCK) affects the antral G-cell. Immunohistochemistry, radioimmunoassay and quantitative real-time polymerase chain reaction techniques were employed to examine the expression of genes belonging to the G-cell secretory pathway in gastrin and gastrin-CCK knockout mice. Transmission electron microscopy was used to examine the ultrastructure of the G-cells. The number of G-cells increased but the secretory granules were few and abnormally small in the G-cells of... (More)
The antral hormone gastrin is the key regulator of gastric acid secretion, mucosal growth and differentiation. Gastrin is synthesized in the endocrine G-cells in the antroduodenal mucosa. We have now examined the way in which the loss of gastrin alone or gastrin plus cholecystokinin (CCK) affects the antral G-cell. Immunohistochemistry, radioimmunoassay and quantitative real-time polymerase chain reaction techniques were employed to examine the expression of genes belonging to the G-cell secretory pathway in gastrin and gastrin-CCK knockout mice. Transmission electron microscopy was used to examine the ultrastructure of the G-cells. The number of G-cells increased but the secretory granules were few and abnormally small in the G-cells of both mouse models compared with wildtypes. Thus, gastrin is not necessary for the formation of G-cells as such but the lack of gastrin reduces the number and size of their secretory granules suggesting that gastrin is vital for the formation and/or maintenance of secretory granules in G-cells. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
transgenic mice, ultrastructure, G-cells, secretion, gastrin, cholecystokinin
in
Cell and Tissue Research
volume
321
issue
1
pages
141 - 146
publisher
Springer
external identifiers
  • pmid:15906100
  • wos:000230317000015
  • scopus:22144441290
ISSN
1432-0878
DOI
10.1007/s00441-005-1110-z
language
English
LU publication?
yes
id
b7dc7a09-1753-4b74-94cb-510a300d2b95 (old id 233540)
date added to LUP
2007-08-02 16:23:05
date last changed
2017-01-01 04:40:19
@article{b7dc7a09-1753-4b74-94cb-510a300d2b95,
  abstract     = {The antral hormone gastrin is the key regulator of gastric acid secretion, mucosal growth and differentiation. Gastrin is synthesized in the endocrine G-cells in the antroduodenal mucosa. We have now examined the way in which the loss of gastrin alone or gastrin plus cholecystokinin (CCK) affects the antral G-cell. Immunohistochemistry, radioimmunoassay and quantitative real-time polymerase chain reaction techniques were employed to examine the expression of genes belonging to the G-cell secretory pathway in gastrin and gastrin-CCK knockout mice. Transmission electron microscopy was used to examine the ultrastructure of the G-cells. The number of G-cells increased but the secretory granules were few and abnormally small in the G-cells of both mouse models compared with wildtypes. Thus, gastrin is not necessary for the formation of G-cells as such but the lack of gastrin reduces the number and size of their secretory granules suggesting that gastrin is vital for the formation and/or maintenance of secretory granules in G-cells.},
  author       = {Friis-Hansen, L and Wierup, Nils and Rehfeld, J F and Sundler, Frank},
  issn         = {1432-0878},
  keyword      = {transgenic mice,ultrastructure,G-cells,secretion,gastrin,cholecystokinin},
  language     = {eng},
  number       = {1},
  pages        = {141--146},
  publisher    = {Springer},
  series       = {Cell and Tissue Research},
  title        = {Antral G-cell in gastrin and gastrin-cholecystokinin knockout animals},
  url          = {http://dx.doi.org/10.1007/s00441-005-1110-z},
  volume       = {321},
  year         = {2005},
}