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Gene expression profiling of gastric mucosa in mice lacking CCK and gastrin receptors
Chun-Mei Zhao1, Yosuke Kodama1, Arnar Flatberg1
1Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, 7006 Trondheim, Norway.
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.
Insights
Mice lacking cholecystokinin (CCK) receptors show altered stomach acid production and signaling pathways. This suggests a potential link between gastric hormones, vitamin D, and bone metabolism regulation.
Area of Science:
- Gastroenterology
- Endocrinology
- Bone Biology
Background:
- Gastric acid secretion is crucial for bone homeostasis.
- Cholecystokinin (CCK) receptors play a role in regulating gastric functions.
- The interplay between gastric acid, CCK signaling, and bone metabolism requires further investigation.
Purpose of the Study:
- To investigate the role of CCK1 and CCK2 receptors in gastric acid secretion and related signaling pathways.
- To explore the potential connection between gastric factors and bone metabolism in CCK receptor knockout mice.
Main Methods:
- Utilized CCK1 receptor knockout (KO), CCK2 receptor KO, and CCK1+2 receptor double KO mouse models.
- Assessed gastric acid secretion following pylorus ligation-induced vagal stimulation.
- Examined the expression of signaling molecules like pituitary adenylate cyclase-activating polypeptide type 1 receptor (PAC1), parathyroid hormone-like hormone (PTHLH), and vitamin D3 1α hydroxylase in gastric mucosa.
Main Results:
- CCK2 receptor KO mice exhibited impaired gastric acid secretion and ECL cell signaling.
- CCK1+2 receptor double KO mice showed partial normalization of acid secretion and ECL cell pathway, associated with increased PAC1 receptor expression.
- Gastric mucosa expressed PTHLH and vitamin D3 1α hydroxylase, suggesting a potential role in gastric-bone axis regulation.
Conclusions:
- Absence of CCK receptors induces a functional shift from gastrin-CCK pathways to neuronal control of gastric acid secretion.
- A potential link exists between gastric parathyroid hormone-like hormone (PTHLH), vitamin D metabolism, and bone homeostasis.
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