The effects of rabeprazole on ECL cells and parietal cells in rat -comparison with omeprazole

2000 ◽  
Vol 118 (4) ◽  
pp. A1110
Author(s):  
Akira Tari ◽  
Masanori Kawano ◽  
Toyohiko Aoki ◽  
Yoshikazu Yonei ◽  
Kanji Kodama ◽  
...  
Keyword(s):  
Parietal Cells ◽  
Ecl Cells

scholarly journals Purification of Gastric Mucosal ECL Cells from a Crude Elutriation Fraction

2002 ◽  
Vol 2 ◽  
pp. 1643-1645 ◽  
Author(s):  
John Graham
Keyword(s):  
Gastric Mucosa ◽  
Ion Transport ◽  
Parietal Cell ◽  
Cell Function ◽  
Parietal Cells ◽  
Centrifugal Elutriation ◽  
Ecl Cells ◽  
Acid Secreting ◽  
Density Barrier

Acid-secreting parietal cells from the gastric mucosa are widely studied as a model in studies on ion transport and the endocrine/paracrine ECL cells effectively control parietal cell function. Discontinuous gradients of iodixanol for the purification of ECL cells were subsequently simplified to the use of a density barrier. This technique is now commonly used following initial centrifugal elutriation.

Differentiation of the Gastric Mucosa I. Role of histamine in control of function and integrity of oxyntic mucosa: understanding gastric physiology through disruption of targeted genes

2006 ◽  
Vol 291 (4) ◽  
pp. G539-G544 ◽  
Author(s):  
Duan Chen ◽  
Takeshi Aihara ◽  
Chun-Mei Zhao ◽  
Rolf Håkanson ◽  
Susumu Okabe
Keyword(s):  
Gastric Mucosa ◽  
Histidine Decarboxylase ◽  
Parietal Cells ◽  
Oxyntic Mucosa ◽  
Mucosal Integrity ◽  
Ecl Cells ◽  
Gastric Physiology ◽  
Ecl Cell ◽  
Insight Into

Many physiological functions of the stomach depend on an intact mucosal integrity; function reflects structure and vice versa. Histamine in the stomach is synthesized by histidine decarboxylase (HDC), stored in enterochromaffin-like (ECL) cells, and released in response to gastrin, acting on CCK2 receptors on the ECL cells. Mobilized ECL cell histamine stimulates histamine H2 receptors on the parietal cells, resulting in acid secretion. The parietal cells express H2, M3, and CCK2 receptors and somatostatin sst2 receptors. This review discusses the consequences of disrupting genes that are important for ECL cell histamine release and synthesis (HDC, gastrin, and CCK2 receptor genes) and genes that are important for “cross-talk” between H2 receptors and other receptors on the parietal cell (CCK2, M3, and sst2 receptors). Such analysis may provide insight into the functional significance of gastric histamine.

Anatomical location of enterochromaffin-like (ECL) cells, parietal cells, and chief cells in the stomach demonstrated by immunocytochemistry and electron microscopy

1999 ◽  
Vol 34 (3) ◽  
pp. 315-320 ◽  
Author(s):  
Sachiko Kamoshida ◽  
Eiichi Saito ◽  
Satoru Fukuda ◽  
Kimitoshi Kato ◽  
Ariyoshi Iwasaki ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Parietal Cells ◽  
Anatomical Location ◽  
Chief Cells ◽  
Ecl Cells

Impaired gastric acid secretion in gastrin-deficient mice

1998 ◽  
Vol 274 (3) ◽  
pp. G561-G568 ◽  
Author(s):  
Lennart Friis-Hansen ◽  
Frank Sundler ◽  
Ying Li ◽  
Patrick J. Gillespie ◽  
Thomas L. Saunders ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Histidine Decarboxylase ◽  
Embryonic Stem ◽  
Parietal Cells ◽  
Gastric Glands ◽  
Partial Restoration ◽  
Ecl Cells ◽  
Deficient Mice

To further understand the role of the peptide hormone gastrin in the development and function of the stomach, we have generated gastrin-deficient mice by gene targeting in embryonic stem cells. Mutant mice were viable and fertile, without obvious visible abnormalities. However, gastric function was severely affected by the loss of gastrin. Basal gastric acid secretion was abolished and could not be induced by histamine, carbachol, or gastrin. Histological analysis revealed alterations in the two cell types primarily involved in acid secretion, parietal and enterochromaffin-like (ECL) cells. Parietal cells were reduced in number with an accumulation of immature cells lacking H+-K+-adenosinetriphosphatase (H+-K+-ATPase). ECL cells were positioned closer to the base of the gastric glands, with markedly lower expression of histidine decarboxylase. Gastrin administration for 6 days reversed the effects of the gastrin deficiency, leading to an increase in the number of mature, H+-K+-ATPase-positive parietal cells and a partial restoration of acid secretion. The results show that gastrin is critically important for the function of the acid secretory system.

scholarly journals Control of Gastric Acid Secretion in Somatostatin Receptor 2 Deficient Mice: Shift from Endocrine/Paracrine to Neurocrine Pathways

Endocrinology ◽  
2007 ◽  
Vol 149 (2) ◽  
pp. 498-505 ◽  
Author(s):  
Chun-Mei Zhao ◽  
Vicente Martinez ◽  
Laura Piqueras ◽  
Lixin Wang ◽  
Yvette Taché ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Knockout Mice ◽  
Somatostatin Receptor ◽  
Parietal Cells ◽  
Receptor Type ◽  
Oxyntic Mucosa ◽  
Gastrin Cells ◽  
Ecl Cells

The gastrin-enterochromaffin-like (ECL) cell-parietal cell axis is known to play an important role in the regulation of gastric acid secretion. Somatostatin, acting on somatostatin receptor type 2 (SSTR2), interferes with this axis by suppressing the activity of the gastrin cells, ECL cells, and parietal cells. Surprisingly, however, freely fed SSTR2 knockout mice seem to display normal circulating gastrin concentration and unchanged acid output. In the present study, we compared the control of acid secretion in these mutant mice with that in wild-type mice. In SSTR2 knockout mice, the number of gastrin cells was unchanged; whereas the numbers of somatostatin cells were reduced in the antrum (−55%) and increased in the oxyntic mucosa (35%). The ECL cells displayed a reduced expression of histidine decarboxylase and vesicle monoamine transport type 2 (determined by immunohistochemistry), and an impaired transformation of the granules to secretory vesicles (determined by electron microscopic analysis), suggesting low activity of the ECL cells. These changes were accompanied by an increased expression of galanin receptor type 1 in the oxyntic mucosa. The parietal cells were found to respond to pentagastrin or to vagal stimulation (evoked by pylorus ligation) with increased acid production. In conclusion, the inhibitory galanin-galanin receptor type 1 pathway is up-regulated in the ECL cells, and the direct stimulatory action of gastrin and vagal excitation is enhanced on the parietal cells in SSTR2 knockout mice. We suggest that there is a remodeling of the neuroendocrine mechanisms that regulate acid secretion in these mutant mice.

Role of neuropeptide-sensitive L-type Ca2+ channels in histamine release in gastric enterochromaffin-like cells

1999 ◽  
Vol 277 (6) ◽  
pp. G1268-G1280 ◽  
Author(s):  
Ningxin Zeng ◽  
Christoph Athmann ◽  
Tao Kang ◽  
John H. Walsh ◽  
George Sachs
Keyword(s):  
Histamine Release ◽  
Peptide Yy ◽  
Parietal Cells ◽  
Channel Blockade ◽  
Gastric Glands ◽  
Ecl Cells ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Release Histamine ◽  
Cell Depolarization

Peptides release histamine from enterochromaffin-like (ECL) cells because of elevation of intracellular Ca2+concentration ([Ca2+]i) by either receptor-operated or voltage-dependent Ca2+ channels (VDCC). To determine whether VDCCs contribute to histamine release stimulated by gastrin or pituitary adenylate cyclase-activating polypeptide (PACAP), the presence of VDCCs and their possible modulation by peptides was investigated in a 48-h cultured rat gastric cell population containing 85% ECL cells. Video imaging of fura 2-loaded cells was used to measure [Ca2+]i, and histamine was assayed by RIA. Cells were depolarized by increasing extracellular K+ concentrations or by 20 mM tetraethylammonium (TEA+). Cell depolarization increased transient and steady-state [Ca2+]iand resulted in histamine release, dependent on extracellular Ca2+. These K+- or TEA+-dependent effects on histamine release from ECL cells were coupled to activation of parietal cells in intact rabbit gastric glands, and L-type channel blockade by 2 μM nifedipine inhibited 50% of [Ca2+]i elevation and histamine release. N-type channel blockade by 1 μM ω-conotoxin GVIA inhibited 25% of [Ca2+]i elevation and 14% of histamine release. Inhibition was additive. The effects of 20 mM TEA+ were fully inhibited by 2 μM nifedipine. Both classes of Ca2+ channels were found in ECL cells, but not in parietal cells, by RT-PCR. Nifedipine reduced PACAP-induced (but not gastrin-stimulated) Ca2+ entry and histamine release by 40%. Somatostatin, peptide YY (PYY), and galanin dose dependently inhibited L-type Ca2+ channels via a pertussis toxin-sensitive pathway. L-type VDCCs play a role in PACAP but not gastrin stimulation of histamine release from ECL cells, and the channel opening is inhibited by somatostatin, PYY, and galanin by interaction with a Gi or Go protein.

Regulation of parietal cell calcium signaling in gastric glands

2000 ◽  
Vol 279 (5) ◽  
pp. G1048-G1058 ◽  
Author(s):  
Christoph Athmann ◽  
Ningxin Zeng ◽  
David R. Scott ◽  
George Sachs
Keyword(s):  
Calcium Signaling ◽  
Calcium Concentration ◽  
Cellular Responses ◽  
Parietal Cells ◽  
Gastric Glands ◽  
Cell Calcium ◽  
Ecl Cells ◽  
Ecl Cell ◽  
Pituitary Adenylate Cyclase ◽  
Signaling Interactions

The ligands interacting with enterochromaffin-like (ECL) and parietal cells and the signaling interactions between these cells were investigated in rabbit gastric glands using confocal microscopy. Intracellular calcium concentration ([Ca2+]i) changes were used to monitor cellular responses. Histamine and carbachol increased [Ca2+]i in parietal cells. Gastrin (1 nM) increased [Ca2+]i in ECL cells and adjacent parietal cells. Only the increase of [Ca2+]i in parietal cells was inhibited by H2 receptor antagonists (H2RA). Gastrin (10 nM) evoked an H2RA-insensitive [Ca2+]i increase in parietal cells. Carbachol produced large H2RA- and somatostatin-insensitive signals in parietal cells. Pituitary adenylate cyclase-activating peptide (PACAP, 100 nM) elevated [Ca2+]i in ECL cells and adjacent parietal cells. H2RAs abolished the PACAP-stimulated [Ca2+]i increase in adjacent parietal cells. Somatostatin did not inhibit the increase of [Ca2+]i in parietal cells stimulated with histamine, high gastrin concentrations, or carbachol but abolished ECL cell calcium responses to gastrin or PACAP. Hence, rabbit parietal cells express histaminergic, muscarinic, and CCK-B receptors coupled to calcium signaling but insensitive to somatostatin, whereas rabbit and rat ECL cells express PACAP and CCK-B calcium coupled receptors sensitive to somatostatin.

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