Proliferation of enterochromaffinlike cells in omeprazole-treated hypergastrinemic rats

Tielemans, Y.; Håkanson, R.; Sundler, F.; Willems, Glenda

doi:10.1016/0016-5085(89)90895-0

Cited by 71 publications

(51 citation statements)

References 31 publications

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“…Within the gastric mucosa, the ECL cell is known to be particularly susceptible to the trophic effect of gastrin [4, 22]. Consistent with previous investigations in the rat [23], the number of ECL cells increased to a relatively greater extent than did the total number of proliferating epithelial cells.…”

Section: Discussionsupporting

confidence: 79%

“…Whilst the number of apoptotic cells almost doubled, the numbers of proliferative cells increased almost 4-fold. Previously, using tritiated thymidine labeling methods gastric mucosal proliferation was increased by only 20–25% under conditions of hypergastrinemia induced by hypochlorhydria in the rat [4, 22, 23]. These differences may reflect species differences between rat and Mastomys and/or be due to the proliferative index measured by Mib-5 expression being far more sensitive than the thymidine labeling index [24].…”

Section: Discussionmentioning

confidence: 99%

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Gastrin-Mediated Alterations in Gastric Epithelial Apoptosis and Proliferation in a <i>Mastomys</i> Rodent Model of Gastric Neoplasia

Kidd¹,

Tang

Modlin

et al. 2000

Digestion

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Background/Aims: Hypergastrinemia secondary to low acid secretion is associated with gastric carcinoid formation in Mastomys. We investigated the effect of gastrin on oxyntic epithelial apoptosis and proliferation in this model. Methods: Hypergastrinemia and mucosal hyperplasia were induced by irreversible H₂ receptor blockade with loxtidine. Gastrin levels were normalised in some animals by 10 days’ loxtidine withdrawal. Serum gastrin was determined by radioimmunoassay, proliferative, enterochromaffin-like cells and Bcl-2 protein family expression by immunohistochemisty, and apoptotic cells by terminal deoxyuridine nucleotide nick end labeling (TUNEL). Results: Proliferating cells were increased 4-fold in loxtidine-treated animals, and returned to normal upon loxtidine withdrawal. Enterochromaffin-like cell number increased 2-fold with loxtidine, and did not decrease after withdrawal. Apoptotic epithelial cells were located at the luminal surface and increased 1.8-fold with loxtidine, returning to control levels upon withdrawal. The ratio of proliferative to apoptotic cells was lower in the control and withdrawn groups than in the loxtidine group (0.26 ± 0.05 and 0.26 ± 0.08 vs. 0.77 ± 0.12). With hypergastrinemia, the expression of Bcl-2 and Bak was increased and Bax decreased in the middle of the gland. Conclusion: Hypergastrinemia is associated with alterations in both proliferation and apoptosis in Mastomys gastric mucosa. This may contribute to the pathogenesis of mucosal hyperplasia in this model.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Gastrin-Mediated Alterations in Gastric Epithelial Apoptosis and Proliferation in a <i>Mastomys</i> Rodent Model of Gastric Neoplasia

Kidd¹,

Tang

Modlin

et al. 2000

Digestion

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“…no. LSB2, USA) for 21-28 days as previously described [40,41]. The 3H-thyidine labeling index (L.I.)…”

Section: Autoradiographymentioning

confidence: 99%

“…was determined in 4 pm thin. The number of cells incorporating the silver grains was measured in the generative cell zone of the oxyntic mucosa, which was defined as the area between the uppermost parietal cells and the uppermost chief cells in each gland [41]. The sections were stained with Hematoxylin and eosin (HE) stain.…”

Section: Autoradiographymentioning

confidence: 99%

Detection of Cholecystokinin B/Gastrin Receptor mRNA Expressing Cells in the Stomach of Hypergastrinemic Rats.

Kawasaki

Fujimura

Mori

et al. 1995

Acta Histochem. Cytochem

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“…1990). Sustained hypergastrinaemia, resulting from treatment with proton pump inhibitors, induces hypertrophy and hyperplasia of ECL cells (Larsson et al 1986;Tielemans et al 1989Tielemans et al & 1990Hdkanson et al 1993). Gastrin-evoked hyperactivity and hypertrophyihyperplasia of ECL cells are reversed after normalising the serum gastrin concentration (Larsson et al 1988;Tielemans et al 1992).…”

mentioning

confidence: 99%

Reversibility of Cholecystokinin‐B/Gastrin Receptor Blockade: A Study of the Gastrin‐ECL Cell Axis in the Rat

Norlén

Lindström

Ding

et al. 1999

Pharmacology & Toxicology

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Absfract: Gastrin acts via cholecystokinin-Blgastrin receptors to control histamine-and chromogranin A-producing ECL cells, which constitute the quantitatively predominant endocrine cell population in the acid-producing part of the rat stomach. Cholecystokinin-B receptor blockade is known to suppress the activity of ECL cells and to prevent their ability to respond to gastrin stimulation. The present study examines the reversibility of long-standing cholecystokinin-B receptor blockade of ECL cells. YM022, a potent and selective cholecystokinin-B receptor antagonist, was administered in a maximally effective dose by continuous subcutaneous infusion for 4 weeks (via osmotic minipumps). The resulting receptor blockade was manifested in elevated serum gastrin concentration (due to the ensuing acid inhibition), while the serum pancreastatin concentration, oxyntic mucosal histidine decarboxylase activity, histidine decarboxylase-and chromogranin A-mRNA levels and histamine and pancreastatin concentrations were lowered. After withdrawal of YM022, all these parameters returned to normal after varying lengths of time. The serum gastrin concentration and the oxyntic mucosal histidine decarboxylase activity returned to normal within a week after termination of treatment. The serum pancreastatin concentration and the mucosal histidine decarboxylase-and chromogranin A-mRNA levels returned to normal within 2 weeks of drug withdrawal. The mucosal pancreastatin and histamine concentrations remained unchanged for about a week before gradually returning to control levels within the next two weeks. Hence, the various effects of cholecystokinin-B receptor blockade of the ECL cells are fully reversible within 1-3 weeks of drug withdrawal.

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Proliferation of enterochromaffinlike cells in omeprazole-treated hypergastrinemic rats

Cited by 71 publications

References 31 publications

Gastrin-Mediated Alterations in Gastric Epithelial Apoptosis and Proliferation in a <i>Mastomys</i> Rodent Model of Gastric Neoplasia

Gastrin-Mediated Alterations in Gastric Epithelial Apoptosis and Proliferation in a <i>Mastomys</i> Rodent Model of Gastric Neoplasia

Detection of Cholecystokinin B/Gastrin Receptor mRNA Expressing Cells in the Stomach of Hypergastrinemic Rats.

Reversibility of Cholecystokinin‐B/Gastrin Receptor Blockade: A Study of the Gastrin‐ECL Cell Axis in the Rat

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