Disease relevance of Chief Cells, Gastric

• NCX-4016 protected gastric chief cells from toxicity induced by TNF-alpha by activating cGMP-dependent pathways [1].
• Inhibitory action of somatostatin on cAMP dependent pepsinogen secretion from rat gastric chief cells: involvement of pertussis toxin-sensitive G-protein [2].

High impact information on Chief Cells, Gastric

• PGs equipotently stimulated increases in the accumulation of diacylglycerol and cyclic AMP without elevating intracellular Ca2+ concentrations in gastric chief cells [3].
• A primary culture of gastric chief cells was used to investigate whether NCX-4016 modulates guanosine 3',5'-cyclic monophosphate (cGMP)-dependent pathways [1].
• BACKGROUND & AIMS: Although epidermal growth factor (EGF) inhibits gastric acid secretion, the effects it exerts on gastric chief cells are unknown [4].
• METHODS: Isolated gastric chief cells were obtained from guinea pig stomach by collagenase digestion and calcium chelation with ethylene glycol-bis(B-amynomethyl ether)-N,N,N',N'-tetraacetic acid [5].
• To better understand the mechanism by which ethanol causes gastric mucosal injury, the effects of ethanol on isolated guinea pig gastric chief cells were investigated in vitro [6].

Biological context of Chief Cells, Gastric

• For example, gastric chief cells, which contain relatively little F-actin and secrete the enzyme, pepsinogen, by regulated exocytosis, do not appear to express lasp-1 [7].
• Immunohistochemical studies conducted with monoclonal antibodies (mAbs) directed against two TNF receptor associated proteins of 55 kDa (TNF-R1) and 75 kDa (TNF-R2) showed that TNF binding sites were expressed in approximately 100% gastric chief cells [8].
• These observations support the hypothesis that, in gastric chief cells, interplay between calcium/calmodulin binding and phosphorylation of a common domain on the 72-kDa MARCKS-like protein plays a role in modulating pepsinogen secretion [9].
• Exposure of guinea pig gastric chief cells to indomethacin (10 microM) did not reduce cell viability as evaluated by lactate dehydrogenase and 51Cr release and trypan blue incorporation [10].

Anatomical context of Chief Cells, Gastric

• The results indicate, therefore, that on gastric chief cell membranes there exist specific CCK receptors, which are coupled to G protein [11].
• Reappraisal of potassium permanganate oxidation applied to Lowicryl K4M embedded tissues processed by high pressure freezing/freeze substitution, with special reference to differential staining of the zymogen granules of rat gastric chief cells [12].
• Phenanthrenequinone induces moderate to intense fluorescence in gastric chief cells, parenchymal cells of the pancreas, and certain peptide hormone-producing cell types such as the GH cells of the adenohypophysis and the glucagon cells of the pancreatic islets [13].

Associations of Chief Cells, Gastric with chemical compounds

• The aim of this study was to examine the distribution of rab3D, a low-molecular-weight guanosine 5'-triphosphate-binding protein, in gastric chief cells [14].
• These results suggest that the effect of ethanol on pepsinogen release from the gastric chief cells may be due to its opening of a Ca2+ channel that is sensitive to La3+ and that the pepsinogen releasing action of ethanol may be one of factors for ethanol-induced gastric mucosal injury [6].
• Electrical effects of histamine on monolayers formed in culture from enriched canine gastric chief cells [15].
• These results indicate that guanine nucleotides activate major signaling pathways in gastric chief cells [16].
• In cholera toxin-treated gastric chief cells, incubation with a cholinergic agonist (carbamylcholine), a regulatory peptide (cholecystokinin), or a calcium ionophore (A23187) causes a dose- and time-dependent potentiation of cAMP levels [17].

Gene context of Chief Cells, Gastric

• Cholinergic agonist-induced pepsinogen secretion from murine gastric chief cells is mediated by M1 and M3 muscarinic receptors [18].
• These data clearly indicate that, in gastric chief cells, a mixture of M1 and M3 receptors mediates cholinergic stimulation of pepsinogen secretion and that no other muscarinic receptor subtypes are involved in this activity [18].
• Functional localization of proprotein-convertase furin and its substrate TGFbeta in EGF receptor-expressing gastric chief cells [19].
• Gastric chief cells were isolated from the rat stomach in an attempt to identify those involved in the mechanism of action of somatostatin on pepsinogen secretion [20].
• In gastric chief cells, PYY and NPY attenuate the stimulatory effects of secretagogues whose actions are mediated by changes in cellular levels of cAMP [21].

Analytical, diagnostic and therapeutic context of Chief Cells, Gastric

• We used light microscopy, transmission electron microscopy, and stereological point-counting methods to investigate the response of rat gastric chief cells to corticosterone and thyroxine during postnatal development [22].

References