Disease relevance of Enterochromaffin-like Cells

• Our data indicate that the omeprazole-evoked ECL cell hyperplasia is a result of accelerated self-replication [1].
• Mutations of Reg were identified in 3 of 5 patients with ECL cell carcinoid tumors; in 2 cases, mutation of the initiator methionine residue led to exclusion of the protein from the secretory pathway [2].
• Previous studies have shown that the proinflammatory cytokine interleukin (IL)-1beta present during chronic gastritis inhibits histamine synthesis in ECL cells and leads to sustained functional impairment [3].
• Helicobacter pylori lipopolysaccharide stimulates histamine release and DNA synthesis in rat enterochromaffin-like cells [4].
• E. coli LPS had a weak stimulatory effect on ECL cell BrdU uptake at 10(-6) mol/L but had no effect on gastrin-stimulated BrdU uptake [4].

High impact information on Enterochromaffin-like Cells

• Expression of PAC1 splice variants in purified ECL cells was determined by RT-PCR [5].
• PACAP-27 and -38 dose-dependently raise [Ca(2+)](i) in ECL cells, and stimulated histamine release [5].
• BACKGROUND & AIMS: Three pathways control gastric acid secretion: the gastrin-enterochromaffin-like (ECL) cell axis, the vagus-parietal cell axis, and the cholecystokinin (CCK)-D cell axis [6].
• BACKGROUND & AIMS: Gastrin stimulation of the type 2 cholecystokinin (CCK(2)) receptor results in ECL cell proliferation and histamine secretion [7].
• The activity of the histamine forming enzyme, histidine decarboxylase (a marker of ECL cells), was undetectable in the oxyntic mucosa of KO mice yet was readily apparent in the mucosa from WT animals [7].

Chemical compound and disease context of Enterochromaffin-like Cells

• Copresence of prostaglandin EP2 and EP3 receptors on gastric enterochromaffin-like cell carcinoid in African rodents [8].
• CONCLUSION: Corpus enterochromaffin-like cell increases were related to serum gastrin elevation, but neither H. pylori nor long-term treatment with lansoprazole alone or together had any effect on enterochromaffin-like cell density or hyperplasia [9].
• Time-course changes of ECL cell markers in acetic acid-induced gastric ulcers in rats [10].
• Hypergastrinemia, ECL cell hyperplasia, and cell proliferation are significantly inhibited by in vivo blockade of somatostatin receptors by administration of octreotide [11].
• In the African rodent (mastomys) hypergastrinemia generated by the histamine-2 receptor antagonist (loxtidine) results in ECL cell hyperplasia and neoplasia at 8 and 16 weeks respectively [12].

Biological context of Enterochromaffin-like Cells

• The ECL cells were purified, and cell proliferation at each stage in response to gastrin and TGF alpha was measured by bromodeoxyuridine uptake [13].
• We have shown that Reg gene expression is increased in enterochromaffin-like (ECL) cells during the healing of damaged gastric mucosa around mucosal erosion [14].
• CONCLUSIONS: These data suggest that IL-1beta induces programmed cell death in isolated rat ECL cells via activation of NF-kappaB, iNOS, and the Bax protein [3].
• RESULTS: Polymerase chain reaction performed with templates from an ECL cell complementary DNA library and primers specific to each of the five known somatostatin receptor subtypes showed that the somatostatin receptor type 2 was significantly enriched in ECL complementary DNA [15].
• CONCLUSIONS: Gastrin stimulates the production of Reg protein in gastric ECL cells, which may be involved in the gastrin-induced gastric mucosal cell growth [16].

Anatomical context of Enterochromaffin-like Cells

• PACAP type I receptor activation regulates ECL cells and gastric acid secretion [5].
• BACKGROUND & AIMS: Enterochromaffin-like (ECL) cells are histamine-containing endocrine cells in the gastric mucosa [3].
• RESULTS: Gastrin reduced the number of cytoplasmic vesicles in ECL cells while reducing the concentrations of histamine and pancreastatin in the oxyntic mucosa [17].
• CONCLUSIONS: Activation of a Y1 inhibitory receptor subtype present on the gastric ECL cell that inhibits gastrin-induced ECL cell histamine release and Ca2+ entry by activation of a Gi or G(o) class of protein may account for inhibition of gastric acid secretion by PYY released from the small intestine [18].
• In contrast, in the glandular stomach, the differentiation of the gastrin- (G cells) and somatostatin (D cells)-secreting cells is impaired whereas serotonin- (enterochromaffin EC cells), histamine- (enterochromaffin-like ECL cells) and ghrelin (X/A cells)-expressing cells are still present [19].

Associations of Enterochromaffin-like Cells with chemical compounds

• A progressive increase in the ECL cell labeling index was observed from the second day of omeprazole treatment [1].
• Before surgery, octreotide was infused for 72 hours to suppress enterochromaffin-like (ECL) cell and gastrin cell function [20].
• The M1 muscarinic receptor antagonist pirenzepine dose dependently inhibited the action of acetylcholine, whereas the M3 receptor antagonist 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride had no effect. the rest of the evaluated agents had no effect on ECL cell histamine secretion [21].
• METHODS: Using a rat ECL cell preparation of high purity (+/-95%), basal and stimulated histamine secretion and DNA synthesis were measured by enzyme immunoassay and bromodeoxyuridine (BrdU) uptake, respectively [4].
• RESULTS: All enterochromaffin-like cells respond to cholecystokinin-B receptor stimulation, but only a few respond to carbachol [22].

Gene context of Enterochromaffin-like Cells

• Pituitary adenylate cyclase activating polypeptide (PACAP) is present in gastric nerves, and PACAP receptors (PAC1) are found on gastric enterochromaffin-like (ECL) cells [5].
• CONCLUSIONS: NGASP stimulates histamine release from ECL cells, but the release is not mediated via CCK-B/gastrin receptor [23].
• CXCR-2 was identified in isolated ECL cells [14].
• The regulation of gastric acid secretion is achieved in the periphery by interplay between three major gastric endocrine cells: the enterochromaffin-like (ECL) cell, the gastrin or G cell, and the somatostatin or D cell [24].
• Expression of the endocytic proteins dynamin and amphiphysin in rat gastric enterochromaffin-like cells [25].

Analytical, diagnostic and therapeutic context of Enterochromaffin-like Cells

• Immunocytochemistry for histamine was used to determine the ECL cell density and combined with [H3]-thymidine autoradiography to establish the labeling index (LI), i.e., the proportion of the ECL cells that has incorporated [H3]thymidine [26].
• Amphiphysin-1 and -2 were also detected in enterochromaffin-like cells by immunohistochemistry in the same locations as dynamin-1 and -2 [25].
• Three to eight weeks after surgery the histamine-storing cells (enterochromaffin-like cells) of the oxyntic mucosa were analysed by fluorescence histochemistry, light and (quantitative) electron microscopy, and fluorometric determination of amines [27].
• Therefore, we describe here a single-step method for isolation of poly(A)+ mRNA from brain capillaries or ECL cells using proteinase K/sodium dodecyl sulfate cell lysis and oligo-deoxythymidine cellulose affinity chromatography [28].
• In situ hybridization clarified that gastrin receptor mRNA was expressed mainly in enterochromaffin-like (ECL) cells in adult rat gastric mucosa [29].

References