Cellular expression of CCK-A and CCK-B/gastrin receptors in human gastric mucosa

Schmitz, Frank; Göke, Michael; Otte, Jan-Michel; Schrader, Henning; Reimann, Babette; Kruse, Marie‐Luise; Siegel, Erhard; Peters, J. H.; Herzig, Karl‐Heinz; Fölsch, Ulrich R.; Schmidt, Wolfgang E.

doi:10.1016/s0167-0115(01)00307-x

Cited by 71 publications

(52 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Expression of CCK-2R in antral gastric tissue has previously been established to be present on chromogranin Apositive neuroendocrine cells sparsely distributed within gastric glands (40). It was determined that CCK-2R staining in the epithelial cells of H. pylori-infected human gastric tissue was significantly higher than in similar H. pylori-noninfected tissue (P < 0.04; Fig.…”

Section: Resultsmentioning

confidence: 87%

Helicobacter pylori Can Induce Heparin-Binding Epidermal Growth Factor Expression via Gastrin and Its Receptor

Dickson¹,

Grabowska²,

El–Zaatari³

et al. 2006

Cancer Research

View full text Add to dashboard Cite

Both gastrin and Helicobacter pylori have been shown capable of up-regulating gene expression and protein shedding of heparin-binding epidermal growth factor (HB-EGF). Furthermore, the bacteria have previously been shown to induce serum hypergastrinemia in infected individuals. The aim of this work was to assess the extent to which the ability of H. pylori to upregulate expression of HB-EGF can be attributed to its effect on gastrin. Gastric cells, transfected with either gastrin small interfering RNA or antisense plasmid or the gastrin/cholecystokinin-2 receptor (CCK-2R), were cultured for 24 hours with H. pylori +/À , a CCK-2R antagonist. Gene expression levels were measured using reverse transcription-PCR, whereas protein changes were measured using ELISA, Western blotting, and immunofluorescence. H. pylori induced significantly higher levels of HB-EGF gene expression and ectodomain shedding in the CCK-2R-transfected cells than the vector control (P < 0.01). Addition of the CCK-2R inhibitor significantly decreased gene and shedding up-regulation. Gastrin down-regulation reduced the effect of the bacteria on HB-EGF gene and protein expression levels. Endogenous gastrin and CCK-2R expression were also found to be significantly up-regulated in all cell lines as a result of exposure to H. pylori (P < 0.02). Gastric mucosal tissue from H. pylori-infected individuals had significantly higher CCK-2R expression levels than noninfected (P < 0.003), and in hypergastrinemic mice, there was an increase in HB-EGF-expressing cells in the gastric mucosa and colocalization of HB-EGF with CCK-2R-positive enterochromaffin-like cells. In conclusion, gastrin and the CCK-2R play significant roles in the induction of HB-EGF gene and protein expression and ectodomain shedding by H. pylori. (Cancer Res 2006; 66(15): 7524-31)

show abstract

Section: Resultsmentioning

confidence: 87%

Helicobacter pylori Can Induce Heparin-Binding Epidermal Growth Factor Expression via Gastrin and Its Receptor

Dickson¹,

Grabowska²,

El–Zaatari³

et al. 2006

Cancer Research

View full text Add to dashboard Cite

show abstract

“…In addition to detection on parietal and chief cells in the guinea pig stomach, CCK2R was also detected on rare unidentified endocrine cells that were negative for gastrin, histamine, secretin, somatostatin, enkephalin, and gastrin-releasing peptide (521). Precise cellular localization of human stomach CCK2R by in situ RT-PCR and immunohistochemistry demonstrated expression in gastric parietal, ECL, and putative precursor cells (261,451). Expression of CCK1R was visualized in neuroendocrine D cells in antral mucosa and in nonparietal cells of the oxyntic mucosa, most likely chief cells, mucous cells, and undifferentiated precursor cells of the stem cell compartment of the oxyntic gland (451).…”

Section: Stomachmentioning

confidence: 92%

Cholecystokinin and Gastrin Receptors

Dufresne

Seva²,

Fourmy³

2006

Physiological Reviews

422

418

View full text Add to dashboard Cite

Cholecystokinin and gastrin receptors (CCK1R and CCK2R) are G protein-coupled receptors that have been the subject of intensive research in the last 10 years with corresponding advances in the understanding of their functioning and physiology. In this review, we first describe general properties of the receptors, such as the different signaling pathways used to exert short- and long-term effects and the structural data that explain their binding properties, activation, and regulation. We then focus on peripheral cholecystokinin receptors by describing their tissue distribution and physiological actions. Finally, pathophysiological peripheral actions of cholecystokinin receptors and their relevance in clinical disorders are reviewed.

show abstract

“…It is reported that CCK may act preferably on CCK1 receptors of D cells to trigger somatostatin release, resulting in the inhibition of gastric acid secretion in rats (Lloyd et al 1992a), dogs (Lloyd et al 1994), and humans (Buchan et al 1993;Schmidt et al 1994). One histochemical study was able to detect the expression of CCK1 receptors in some D cells of the human stomach (Schmitz et al 2001) whereas another immunostaining reported that most of the gastric D cells in the dog and guinea pig were immunoreactive for the CCK2 receptor (Helander et al 1997). In accordance with immunohistochemical findings in the rat stomach (Patterson et al 2001;Sternini et al 1999), we failed to find D cells or other endocrine cell types expressing CCK1 receptors in the gastric fundus and antrum of mice.…”

Section: Cck1 Receptors In Gallbladder and Gastric Mucosamentioning

confidence: 99%

Cellular and subcellular localization of cholecystokinin (CCK)-1 receptors in the pancreas, gallbladder, and stomach of mice

Konno

Takahashi-Iwanaga

Uchigashima

et al. 2014

Histochem Cell Biol

View full text Add to dashboard Cite

show abstract

Cellular expression of CCK-A and CCK-B/gastrin receptors in human gastric mucosa

Cited by 71 publications

References 25 publications

Helicobacter pylori Can Induce Heparin-Binding Epidermal Growth Factor Expression via Gastrin and Its Receptor

Helicobacter pylori Can Induce Heparin-Binding Epidermal Growth Factor Expression via Gastrin and Its Receptor

Cholecystokinin and Gastrin Receptors

Cellular and subcellular localization of cholecystokinin (CCK)-1 receptors in the pancreas, gallbladder, and stomach of mice

Contact Info

Product

Resources

About