scholarly journals The Enterochromaffin-like [ECL] Cell—Central in Gastric Physiology and Pathology

2019 ◽  
Vol 20 (10) ◽  
pp. 2444 ◽  
Author(s):  
Helge L. Waldum ◽  
Øystein F. Sørdal ◽  
Patricia G. Mjønes
Keyword(s):  
Acid Secretion ◽  
Gastric Acid ◽  
Antral Mucosa ◽  
Oxyntic Mucosa ◽  
Trophic Effect ◽  
Gastric Physiology ◽  
Ecl Cell ◽  
Long Time ◽  
Gastric Neoplasia

Background: Studies on the regulation of gastric and pancreatic secretion began more than 100 years ago. Secretin was the first hormone postulated to exist, initiating the field of endocrinology. Gastrin produced in the antral mucosa was the second postulated hormone, and together with histamine and acetylcholine, represent the three major gastric acid secretagogues known since 1920. For a long time, the mast cell was the only recognized histamine-producing cell in the oxyntic mucosa and, in the mid-1980s, the ECL cell was recognized as the cell producing histamine, taking part in the regulation of gastric acid secretion. Methods: This review is based upon literature research and personal knowledge. Results: The ECL cell carries the gastrin receptor, and gastrin regulates its function (histamine release) as well as proliferation. Long-term hypergastrinemia results in gastric neoplasia of variable malignancies, implying that gastric hypoacidity resulting in increased gastrin release will induce gastric neoplasia, including gastric cancer. Conclusions: The trophic effect of gastrin on the ECL cell has implications to the treatment with inhibitors of acid secretion.

Does long-term profound inhibition of gastric acid secretion increase the risk of ECL cell-derived tumors in man?

2016 ◽  
Vol 51 (7) ◽  
pp. 767-773 ◽  
Author(s):  
Helge L. Waldum ◽  
Øyvind Hauso ◽  
Eiliv Brenna ◽  
Gunnar Qvigstad ◽  
Reidar Fossmark
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Ecl Cell

Nitric oxide inhibits gastric acid secretion by increasing intraparietal cell levels of cGMP in isolated human gastric glands

2005 ◽  
Vol 289 (6) ◽  
pp. G1061-G1066 ◽  
Author(s):  
Anna Berg ◽  
Stefan Redéen ◽  
Magnus Grenegård ◽  
Ann-Charlott Ericson ◽  
Sven Erik Sjöstrand
Keyword(s):  
Nitric Oxide ◽  
Gastric Mucosa ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Enzymatic Digestion ◽  
Human Gastric Mucosa ◽  
Gastric Glands ◽  
Oxyntic Mucosa ◽  
No Donor

We have previously identified cells containing the enzyme nitric oxide (NO) synthase (NOS) in the human gastric mucosa. Moreover, we have demonstrated that endogenous and exogenous NO has been shown to decrease histamine-stimulated acid secretion in isolated human gastric glands. The present investigation aimed to further determine whether this action of NO was mediated by the activation of guanylyl cyclase (GC) and subsequent production of cGMP. Isolated gastric glands were obtained after enzymatic digestion of biopsies taken from the oxyntic mucosa of healthy volunteers. Acid secretion was assessed by measuring [14C]aminopyrine accumulation, and the concentration of cGMP was determined by radioimmunoassay. In addition, immunohistochemistry was used to examine the localization of cGMP in mucosal preparations after stimulation with the NO donor S-nitroso- N-acetylpenicillamine (SNAP). SNAP (0.1 mM) was shown to decrease acid secretion stimulated by histamine (50 μM); this effect was accompanied by an increase in cGMP production, which was histologically localized to parietal cells. The membrane-permeable cGMP analog dibuturyl-cGMP (db-cGMP; 0.1–1 mM) dose dependently inhibited acid secretion. Additionally, the effect of SNAP was prevented by preincubating the glands with the GC inhibitor 4 H-8-bromo-1,2,4-oxadiazolo[3,4-d]benz[b][1,4]oxazin-1-one (10 μM). We therefore suggest that NO in the human gastric mucosa is of physiological importance in regulating acid secretion. Furthermore, the results show that NO-induced inhibition of gastric acid secretion is a cGMP-dependent mechanism in the parietal cell involving the activation of GC.

Gastrin mediates the gastric mucosal proliferative response to feeding

1996 ◽  
Vol 271 (3) ◽  
pp. G470-G476 ◽  
Author(s):  
G. V. Ohning ◽  
H. C. Wong ◽  
K. C. Lloyd ◽  
J. H. Walsh
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Pancreatic Secretion ◽  
Proliferative Response ◽  
Male Rats ◽  
Oxyntic Mucosa ◽  
Proliferative Zone ◽  
Mucosal Proliferation

The role of endogenous gastrin in oxyntic mucosal proliferation during feeding in the rat was studied by immunoneutralization with a gastrin-specific monoclonal antibody (MAb) (CURE 051091.5). The immunochemical characteristics of this antibody were characterized by competitive radioimmunoassay, and the in vivo immunoneutralizing properties were validated by measuring effects on gastric acid and pancreatic secretion. Oxyntic mucosal proliferation in response to feeding was measured in adult male rats after a 48-h fast using bromodeoxyuridine (BrdU) immunohistochemistry. Gastrin-specific MAb inhibited gastrin-17- but not pentagastrin-stimulated gastric acid secretion and had no effect on cholecystokinin (CCK)-stimulated pancreatic secretion. In contrast, a MAb specific for the common COOH-terminal pentapeptide of gastrin and CCK inhibited gastrin-17- and pentagastrin-stimulated gastric acid secretion and CCK-stimulated pancreatic secretion. Pretreatment with gastrin-specific MAb 8 h before refeeding significantly reduced by 61% the number of BrdU-labeled cells in the oxyntic mucosal proliferative zone compared with control MAb-treated rats. These results demonstrate the importance of endogenous gastrin in the proliferative response of the oxyntic mucosa to feeding in the rat.

scholarly journals Transcriptional profiling of gastrin-regulated genes in mouse stomach

2007 ◽  
Vol 29 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Renu N. Jain ◽  
Linda C. Samuelson
Keyword(s):  
Acid Secretion ◽  
Gastric Acid ◽  
Parietal Cell ◽  
Transcriptional Profiling ◽  
Cell Types ◽  
Polymerase Chain Reaction Analysis ◽  
Ecl Cell ◽  
Severe Impairment ◽  
Basal Acid ◽  
Acid Secreting

Gastrin, a potent stimulator of gastric acid secretion, primarily targets the acid-secreting parietal cells and histamine-secreting enterochromaffin-like (ECL) cells in the stomach. Accordingly, gastrin-deficient (GAS-KO) mice have a severe impairment in acid secretion. The aim of this study was to characterize changes in gene expression in GAS-KO mice to identify gastrin-regulated genes and to gain insight into how gastric cell types are regulated by gastrin and acid secretion. Affymetrix microarray analysis of GAS-KO and wild-type mice identified numerous differentially expressed transcripts. The results were compared with GAS-KO mice treated with gastrin to identify genes that were gastrin responsive. Finally, genes that were primarily changed due to gastrin and not hypochlorhydria were identified by comparison to mice that are deficient in both gastrin and cholecystokinin (GAS/CCK-KO), since these mice have restored basal acid secretion. The data were validated by quantitative reverse transcriptase polymerase chain reaction analysis. Interestingly, a number of inflammatory response genes were induced in GAS-KO mice and normalized in GAS/CCK-KO mice, suggesting that they were increased in response to low gastric acid. Moreover, a number of parietal cell transcripts that were downregulated in GAS-KO mice were similarly restored in GAS/CCK-KO mice, suggesting that parietal cell changes were also primarily associated with hypochlorhydria. In contrast, ECL cell genes that were markedly downregulated in GAS-KO mice continued to be reduced in GAS/CCK-KO mice, demonstrating that gastrin coordinately regulates a number of ECL cell genes, including several involved in histamine synthesis and secretion.

Sa1346 HYPERGASTRINEMIA DUE TO P-CAB (AN EXTREMELY POTENT GASTRIC ACID SECRETION SUPPRESSOR) USE CAUSE SEVERELY PARIETAL CELL PROTRUSION AND ECL CELL HYPERPLASIA.

2020 ◽  
Vol 158 (6) ◽  
pp. S-325
Author(s):  
Takuji Yamasaki ◽  
Yoshihiro Akita ◽  
Haruna Miyashita ◽  
Ryosuke Miyazaki ◽  
Yuki Maruyama ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Parietal Cell ◽  
Cell Hyperplasia ◽  
Cell Protrusion ◽  
Ecl Cell

III. Lessons learned from gastrin gene deletion in mice

1999 ◽  
Vol 277 (3) ◽  
pp. G500-G505 ◽  
Author(s):  
Karen L. Hinkle ◽  
Linda C. Samuelson
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Gene Deletion ◽  
Embryonic Stem ◽  
Lessons Learned ◽  
Mouse Mutants ◽  
Functional Maturation ◽  
Ecl Cell ◽  
Secretory System

Gastrin is the principal hormonal inducer of gastric acid secretion. Chronic hypergastrinemia, leading to hypersecretion of gastric acid and increased proliferation of parietal and enterochromaffin-like (ECL) cells, has been well described. In contrast, the physiological consequences of chronic gastrin deficiency had been poorly understood until the recent genetic engineering of mouse mutants containing a gastrin gene deletion by homologous recombination in embryonic stem cells. This themes article describes the consequences of constitutive gastrin deficiency on the development and physiology of the stomach. A lack of gastrin disrupts basal gastric acid secretion and renders the acid secretory system unresponsive to acute histaminergic, cholinergic, and gastrinergic stimulation. The defect in acid secretion is greater than would have been predicted from previous studies in which gastrin action was acutely blocked. Cellular changes include thinning of the gastric mucosa in the gastrin-deficient mice, with a reduction in parietal cells and reduced expression of markers of parietal and ECL cell-differentiated functions. The results suggest that gastrin is required for the functional maturation of the acid-secretory system.

Neuronal nitric oxide synthase: expression in rat parietal cells

2001 ◽  
Vol 280 (2) ◽  
pp. G308-G313 ◽  
Author(s):  
Shyamal Premaratne ◽  
Chun Xue ◽  
John M. McCarty ◽  
Muhammad Zaki ◽  
Robert W. McCuen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Intracellular Signaling ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Parietal Cells ◽  
Nadph Diaphorase ◽  
Rt Pcr ◽  
Oxyntic Mucosa

Nitric oxide synthases (NOS) are enzymes that catalyze the generation of nitric oxide (NO) from l-arginine and require nicotinamide adenine dinucleotide phosphate (NADPH) as a cofactor. At least three isoforms of NOS have been identified: neuronal NOS (nNOS or NOS I), inducible NOS (iNOS or NOS II), and endothelial NOS (eNOS or NOS II). Recent studies implicate NO in the regulation of gastric acid secretion. The aim of the present study was to localize the cellular distribution and characterize the isoform of NOS present in oxyntic mucosa. Oxyntic mucosal segments from rat stomach were stained by the NADPH-diaphorase reaction and with isoform-specific NOS antibodies. The expression of NOS in isolated, highly enriched (>98%) rat parietal cells was examined by immunohistochemistry, Western blot analysis, and RT-PCR. In oxyntic mucosa, histochemical staining revealed NADPH-diaphorase and nNOS immunoreactivity in cells in the midportion of the glands, which were identified as parietal cells in hematoxylin and eosin-stained step sections. In isolated parietal cells, decisive evidence for nNOS expression was obtained by specific immunohistochemistry, Western blotting, and RT-PCR. Cloning and sequence analysis of the PCR product confirmed it to be nNOS (100% identity). Expression of nNOS in parietal cells suggests that endogenous NO, acting as an intracellular signaling molecule, may participate in the regulation of gastric acid secretion.

PACAP stimulates gastric acid secretion in the rat by inducing histamine release

2001 ◽  
Vol 281 (4) ◽  
pp. G997-G1003 ◽  
Author(s):  
Arne K. Sandvik ◽  
Guanglin Cui ◽  
Ingunn Bakke ◽  
Bjørn Munkvold ◽  
Helge L. Waldum
Keyword(s):  
Acid Secretion ◽  
Histamine Release ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Rat Stomach ◽  
Neurohumoral Regulation ◽  
Ecl Cell ◽  
Pituitary Adenylate Cyclase ◽  
Awake Rat

Previous studies have shown that pituitary adenylate cyclase-activating peptide (PACAP) stimulates enterochromaffin-like (ECL) cell histamine release, but its role in the regulation of gastric acid secretion is disputed. This work examines the effect of PACAP-38 on aminopyrine uptake in enriched rat parietal cells and on histamine release and acid secretion in the isolated vascularly perfused rat stomach and the role of PACAP in vagally (2-deoxyglucose) stimulated acid secretion in the awake rat. PACAP has no direct effect on the isolated parietal cell as assessed by aminopyrine uptake. PACAP induces a concentration-dependent histamine release and acid secretion in the isolated stomach, and its effect on histamine release is additive to gastrin. The histamine H2antagonist ranitidine potently inhibits PACAP-stimulated acid secretion without affecting histamine release. Vagally stimulated acid secretion is partially inhibited by a PACAP antagonist. The results from the present study strongly suggest that PACAP plays an important role in the neurohumoral regulation of gastric acid secretion. Its effect seems to be mediated by the release of ECL cell histamine.

Gastric Enterochromaffin-Like Cells and the Regulation of Acid Secretion

Physiology ◽  
1996 ◽  
Vol 11 (2) ◽  
pp. 57-62
Author(s):  
G Sachs ◽  
C Prinz
Keyword(s):  
Cell Growth ◽  
Acid Secretion ◽  
Histamine Release ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Histidine Decarboxylase ◽  
Major Pathway ◽  
Ecl Cell

The interaction of gastrin, somatostatin, and other transmitters at the level of the histamine-containing enterochromaffin (ECL) cell is the major pathway determining rate of gastric acid secretion. Gastrin stimulates ECL cell elevation of [Ca2+]i, synthesis of histidine decarboxylase, histamine release, and cell growth by binding at a cholecystokinin-B receptor. Somatostatin inhibits gastrin-dependent elevation of [Ca2+]i and hence histamine release by binding to stomatostatin receptor 2 subtype.

Partial purification of a novel stimulant of gastric acid secretion from canine non-antral mucosa

Life Sciences ◽  
1986 ◽  
Vol 38 (10) ◽  
pp. 887-894 ◽  
Author(s):  
N.W. Bunnett ◽  
M.S. Orloff ◽  
Y. Coto ◽  
H.J. Corbet ◽  
R. Garcia ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Partial Purification ◽  
Antral Mucosa
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