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Gene expression profiling of gastric mucosa in mice lacking CCK and gastrin receptors

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Harvard

Zhao, C-M, Kodama, Y, Flatberg, A, Beisvag, V, Kulseng, B, Sandvik, AK, Rehfeld, JF & Chen, D 2014, 'Gene expression profiling of gastric mucosa in mice lacking CCK and gastrin receptors', Regulatory Peptides, vol. 192-193, pp. 35-44. https://doi.org/10.1016/j.regpep.2014.08.002

APA

Zhao, C-M., Kodama, Y., Flatberg, A., Beisvag, V., Kulseng, B., Sandvik, A. K., Rehfeld, J. F., & Chen, D. (2014). Gene expression profiling of gastric mucosa in mice lacking CCK and gastrin receptors. Regulatory Peptides, 192-193, 35-44. https://doi.org/10.1016/j.regpep.2014.08.002

CBE

MLA

Vancouver

Zhao C-M, Kodama Y, Flatberg A, Beisvag V, Kulseng B, Sandvik AK et al. Gene expression profiling of gastric mucosa in mice lacking CCK and gastrin receptors. Regulatory Peptides. 2014 Aug 28;192-193:35-44. https://doi.org/10.1016/j.regpep.2014.08.002

Author

Zhao, Chun-Mei ; Kodama, Yosuke ; Flatberg, Arnar ; Beisvag, Vidar ; Kulseng, Bård ; Sandvik, Arne K ; Rehfeld, Jens F ; Chen, Duan. / Gene expression profiling of gastric mucosa in mice lacking CCK and gastrin receptors. In: Regulatory Peptides. 2014 ; Vol. 192-193. pp. 35-44.

Bibtex

@article{c4b3b2a4395a44ebb853feeaf38f566c,
title = "Gene expression profiling of gastric mucosa in mice lacking CCK and gastrin receptors",
abstract = "The stomach produces acid, which may play an important role in the regulation of bone homeostasis. The aim of this study was to reveal signaling pathways in the gastric mucosa that involve the acid secretion and possibly the bone metabolism in CCK1 and/or CCK2 receptor knockout (KO) mice. Gastric acid secretion was impaired and the ECL cell signaling pathway was inhibited in CCK2 receptor KO mice but not in CCK1 receptor KO mice. However, in CCK1+2 receptor double KO mice the acid secretion in response to pylorus ligation-induced vagal stimulation and the ECL cell pathway were partially normalized, which was associated with an up-regulated pituitary adenylate cyclase-activating polypeptide (PACAP) type 1 receptor (PAC1). The basal part of the gastric mucosa expressed parathyroid hormone-like hormone (PTHLH) in a subpopulation of likely ECL cells (and possibly other cells) and vitamin D3 1α hydroxylase probably in trefoil peptide2-immunoreactive cells. In conclusion, mice lacking CCK receptors exhibited a functional shift from the gastrin-CCK pathways to the neuronal pathway in control of the ECL cells and eventually the acid secretion. Taking the present data together with previous findings, we suggest a possible link between gastric PTHLH and vitamin D and bone metabolism.",
author = "Chun-Mei Zhao and Yosuke Kodama and Arnar Flatberg and Vidar Beisvag and B{\aa}rd Kulseng and Sandvik, {Arne K} and Rehfeld, {Jens F} and Duan Chen",
note = "Copyright {\textcopyright} 2014 Elsevier B.V. All rights reserved.",
year = "2014",
month = aug,
day = "28",
doi = "10.1016/j.regpep.2014.08.002",
language = "English",
volume = "192-193",
pages = "35--44",
journal = "Regulatory Peptides",
issn = "0167-0115",
publisher = "Elsevier BV",

}

RIS

TY - JOUR

T1 - Gene expression profiling of gastric mucosa in mice lacking CCK and gastrin receptors

AU - Zhao, Chun-Mei

AU - Kodama, Yosuke

AU - Flatberg, Arnar

AU - Beisvag, Vidar

AU - Kulseng, Bård

AU - Sandvik, Arne K

AU - Rehfeld, Jens F

AU - Chen, Duan

N1 - Copyright © 2014 Elsevier B.V. All rights reserved.

PY - 2014/8/28

Y1 - 2014/8/28

N2 - The stomach produces acid, which may play an important role in the regulation of bone homeostasis. The aim of this study was to reveal signaling pathways in the gastric mucosa that involve the acid secretion and possibly the bone metabolism in CCK1 and/or CCK2 receptor knockout (KO) mice. Gastric acid secretion was impaired and the ECL cell signaling pathway was inhibited in CCK2 receptor KO mice but not in CCK1 receptor KO mice. However, in CCK1+2 receptor double KO mice the acid secretion in response to pylorus ligation-induced vagal stimulation and the ECL cell pathway were partially normalized, which was associated with an up-regulated pituitary adenylate cyclase-activating polypeptide (PACAP) type 1 receptor (PAC1). The basal part of the gastric mucosa expressed parathyroid hormone-like hormone (PTHLH) in a subpopulation of likely ECL cells (and possibly other cells) and vitamin D3 1α hydroxylase probably in trefoil peptide2-immunoreactive cells. In conclusion, mice lacking CCK receptors exhibited a functional shift from the gastrin-CCK pathways to the neuronal pathway in control of the ECL cells and eventually the acid secretion. Taking the present data together with previous findings, we suggest a possible link between gastric PTHLH and vitamin D and bone metabolism.

AB - The stomach produces acid, which may play an important role in the regulation of bone homeostasis. The aim of this study was to reveal signaling pathways in the gastric mucosa that involve the acid secretion and possibly the bone metabolism in CCK1 and/or CCK2 receptor knockout (KO) mice. Gastric acid secretion was impaired and the ECL cell signaling pathway was inhibited in CCK2 receptor KO mice but not in CCK1 receptor KO mice. However, in CCK1+2 receptor double KO mice the acid secretion in response to pylorus ligation-induced vagal stimulation and the ECL cell pathway were partially normalized, which was associated with an up-regulated pituitary adenylate cyclase-activating polypeptide (PACAP) type 1 receptor (PAC1). The basal part of the gastric mucosa expressed parathyroid hormone-like hormone (PTHLH) in a subpopulation of likely ECL cells (and possibly other cells) and vitamin D3 1α hydroxylase probably in trefoil peptide2-immunoreactive cells. In conclusion, mice lacking CCK receptors exhibited a functional shift from the gastrin-CCK pathways to the neuronal pathway in control of the ECL cells and eventually the acid secretion. Taking the present data together with previous findings, we suggest a possible link between gastric PTHLH and vitamin D and bone metabolism.

U2 - 10.1016/j.regpep.2014.08.002

DO - 10.1016/j.regpep.2014.08.002

M3 - Journal article

C2 - 25160855

VL - 192-193

SP - 35

EP - 44

JO - Regulatory Peptides

JF - Regulatory Peptides

SN - 0167-0115

ER -

ID: 44770708