Cholecystokinin-B/gastrin receptors enhance wound healing in the rat gastric mucosa

Schmassmann, Adrian; Reubi, Jean Claude

doi:10.1172/jci8115

Cited by 48 publications

(41 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This rate of movement would seem to be distinct from the rapid epithelial cell migration that is involved in wound healing. However, recent studies suggest that there is expression of the gastrin-cholecystokinin-B receptor by surface epithelial cells after gastric mucosal wounding (16). Whether this is associated with functional control of cell migration in the wounded area is unclear.…”

Section: Discussionmentioning

confidence: 99%

Regulation of parietal cell migration by gastrin in the mouse

Kirton

Wang

Dockray

2002

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

Kirton, C. M., T. Wang, and G. J. Dockray. Regulation of parietal cell migration by gastrin in the mouse. Am J Physiol Gastrointest Liver Physiol 283: G787-G793, 2002. First published April 24, 2002 10.1152/ajpgi.00538.2001.-Recent studies suggest that gastrin regulates parietal cell maturation. We asked whether it also regulates parietal cell life span and migration along the gland. Dividing cells were labeled with 5Ј-bromo-2Ј-deoxyuridine (BrdU), and parietal cells were identified by staining with Dolichos biflorus lectin. Cells positive for D. biflorus lectin and BrdU were reliably identified 10-30 days after BrdU injection in mice in which the gastrin gene had been deleted by homologous recombination (Gas-KO) and wild-type (C57BL/6) mice. The time course of labeling was similar in the two groups. The distribution of BrdU-labeled parietal cells in wild-type mice was consistent with migration to the base of the gland, but in Gas-KO mice, a higher proportion of BrdU-labeled cells was found more superficially 20 and 30 days after BrdU injection. Conversely, in transgenic mice overexpressing gastrin, BrdU-labeled parietal cells accounted for a higher proportion of the labeled pool in the base of the gland 10 days after BrdU injection. Gastrin, therefore, stimulates movement of parietal cells along the gland axis but does not influence their life span. gastric epithelium; cell migration; bromodeoxyuridine THE ORGANIZATION OF THE EPITHELIUM throughout the gut is maintained by cellular proliferation followed by migration and differentiation. Proliferating cells in the gastric epithelium are located in the isthmus region of the glands (7). Cells that leave the cell cycle may migrate toward the surface, adopting a mucus-secreting phenotype, or toward the base of the gland, where the main differentiated cell types are parietal, chief, and endocrine cells. In addition, the latter cell types migrate to arrange themselves in characteristic tubular ensembles that constitute the gastric glands. This process is thought to depend on cell-cell and cell-matrix interactions, but little is known of the relevant regulatory mechanisms.It is well recognized that gastrin influences the organization of the gastric epithelium and acutely regulates acid secretion (17). Elevated plasma gastrin concentrations are associated with increased parietal cell mass (15) and hyperplasia of histamine-producing enterochromaffin-like cells (1,12,14). Mice in which the gastrin gene has been deleted by homologous recombination (Gas-KO) are achlorhydric and do not respond to acute administration of the acid secretagogues gastrin, histamine, and carbachol (6). They do, however, secrete acid after treatment with gastrin for Ն24 h (2, 6). These observations, therefore, suggest that gastrin plays a role in parietal cell maturation. Interestingly, in transgenic mice with moderate hypergastrinemia (Ins-Gas mice), there is an initial increase in parietal cell numbers, although this is followed (Ͼ4 mo) by a progressive loss of glandular cells and foveolar hype...

show abstract

Section: Discussionmentioning

confidence: 99%

Regulation of parietal cell migration by gastrin in the mouse

Kirton

Wang

Dockray

2002

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

show abstract

“…The time points were determined from previous studies in rats (11,(23)(24)(25)(26) and preliminary studies using this mouse ulcer model. In preliminary studies in wild-type mice studied on days 1-7, and 10, the mRNA levels of COX and NOS isoforms and epithelial cell proliferation in the mucosal ulcer margin peaked on day 4 and the microvessel density in the ulcer bed peaked on day 7. mRNA levels and epithelial cell proliferation in the ulcer margin showed the most significant differences between wild-type and COX-2 Ϫ/Ϫ mice on day 4.…”

Section: Methodsmentioning

confidence: 99%

Role of the different isoforms of cyclooxygenase and nitric oxide synthase during gastric ulcer healing in cyclooxygenase-1 and -2 knockout mice

Schmassmann¹,

Zoidl²,

Peskar³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

Self Cite

View full text Add to dashboard Cite

show abstract

“…It is noteworthy that gastrin does not act as a trophic agent in the rat stomach before weaning (45). In vivo and in vitro data also suggested that CCK2R, in regenerative rat gastric oxyntic mucosa, enhances trophic effects during gastric wound healing (448). Finally, while it is clear that CCK2R is expressed by parietal and ECL cells, the presence of this receptor on the gastric proliferating progenitor cell population remains to be confirmed, and gastrin is actually considered to act indirectly via the release of growth factors such as HB-EGF and Reg (20,327,540).…”

Section: Stomachmentioning

confidence: 99%

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

Cholecystokinin-B/gastrin receptors enhance wound healing in the rat gastric mucosa

Cited by 48 publications

References 40 publications

Regulation of parietal cell migration by gastrin in the mouse

Regulation of parietal cell migration by gastrin in the mouse

Role of the different isoforms of cyclooxygenase and nitric oxide synthase during gastric ulcer healing in cyclooxygenase-1 and -2 knockout mice

Cholecystokinin and Gastrin Receptors

Contact Info

Product

Resources

About