Disease relevance of Parietal Cells, Gastric

• Achlorhydria by ezrin knockdown: defects in the formation/expansion of apical canaliculi in gastric parietal cells [1].
• Bioactivity studies demonstrated that neither gastrotropin nor a carboxyl-terminally amidated tridecapeptide fragment deduced from the cDNA sequence influence acid secretory activity in rats with gastric fistulas or in isolated canine gastric parietal cells [2].
• Atrophic gastritis was found in all five patients whose sera contained gastric parietal cell antibody and in three of 11 patients with no antibody in their sera [3].
• The reactivity of human pernicious anemia serum with gastric parietal cells could not be inhibited with saccharide inhibitors and, in addition, no binding was observed with normal human sera [4].
• Human sera from autoimmune gastritis patients containing autoantibodies to gastric parietal cells were analyzed by immunological methods [5].

Psychiatry related information on Parietal Cells, Gastric

• Patients with dementia showed an increase of antibody-positive sera against nuclear antigen, gastric parietal cells, CNS antigen, gangliosides (Gm1), laminin, and keratin [6].

High impact information on Parietal Cells, Gastric

• Activation of apical chloride channels in the gastric oxyntic cell [7].
• The activation of oxyntic cell HIP by gastrin was neutralized by an antiserum directed towards the COOH-terminus of gastrin and not by nonimmune serum [8].
• It is thus a measure of hydroxyl ions produced during stimulation of the oxyntic cell and reflects upon hydrogen ion production [8].
• Although histamine does not require extracellular or membrane calcium events to stimulate the oxyntic cell, calmodulin appears to participate in histamine action [9].
• Histamine (10(-17)-10(-14) M), carbamylcholine (10(-12)-10(-9) M), and extracellular calcium (10(-7)-10(-3) M) caused a linear, dose-dependent stimulation of the oxyntic cell [9].

Chemical compound and disease context of Parietal Cells, Gastric

• With the exception of a weakly positive gastric parietal cell antibody test in one of the 12 patients with chronic atrophic gastritis, autoantibodies were not found in all the gastritis and contol groups [10].
• The prevalence of auto-antibodies against thyroid constituents, gastric parietal cells, smooth muscle cells, mitochondria, reticulin, nuclear constituents and rheumatoid factor in 108 patients with alopecia areata was compared with that found in a previous survey of the local population [11].
• These results suggest that TY-11345 has potent antisecretory and antiulcer effects which are exerted by suppression of H+/K(+)-ATPase activity in gastric parietal cells, so that TY-11345 should be useful for the clinical treatment of peptic ulcer diseases [12].
• A 26-year-old woman with congenital myasthenia gravis and antibodies to the acetylcholine receptor developed overt insulin-dependent diabetes with positive islet cell antibodies and thyroid microsomal and gastric parietal cell antibodies [13].

Biological context of Parietal Cells, Gastric

• Action of gastrin in guinea pig oxyntic cells. Studies using quantitative cytochemistry [8].
• Role of cyclic 3',5'-AMP-dependent phosphorylation of membrane proteins in the activation of oxyntic cells [14].
• The 5'-flanking region of the (H+ + K+)-ATPase gene contains potential binding sites for RNA polymerase II and various transcriptional regulation factors and several direct and inverted repeat sequences which may be important for specific and controlled expression of the gene in gastric parietal cells [15].
• In summary, cagE presence appears to be essential for H. pylori-induced apoptosis of gastric parietal cells, and this effect is dependent on the activation of NF-kappaB and production of nitric oxide [16].
• The interaction of the muscarinic agonist carbachol and of dibutyryl cAMP on acid secretion and phosphoinositide second messenger metabolism were studied in rat gastric parietal cells [17].

Anatomical context of Parietal Cells, Gastric

• A single class of voltage-dependent, inwardly rectifying chloride channels was observed in the apical membranes of both resting and stimulated (acid-secreting) oxyntic cells [7].
• The H,K-adenosine triphosphatase (ATPase) of gastric parietal cells is targeted to a regulated membrane compartment that fuses with the apical plasma membrane in response to secretagogue stimulation [18].
• These mice develop autoantibodies to the gastric parietal cell proton pump, H/K ATPase, and aberrant expression of the H/K ATPase in the neonatal thymus prevents the induction of disease post-thymectomy [19].
• Somatostatin inhibits gastric acid secretion in vivo by effects on oxyntic cells which may be indirect [20].
• Pancreatic islet cell, thyroid, gastric parietal cell, and adrenal autoantibodies were studied in 110 young insulin-dependent diabetics (type I; IDDM), 12 non-insulin-dependent diabetics (NIDDM), 26 patients with pancreatic diabetes, and 123 age- and sex-matched healthy controls [21].

Associations of Parietal Cells, Gastric with chemical compounds

• The role of calcium in stimulation of the oxyntic cell by histamine and carbamylcholine was studied using a sensitive quantitative cytochemical staining technique that measures oxyntic cell hydroxyl ion production (HIP) as an index of acid secretion [9].
• Furthermore, direct evidence was obtained from the imaging of the fluorescence that omeprazole was activated in the acidic compartments of the isolated Xenopus oxyntic cell [22].
• The fact that acid output was inhibited during pentagastrin administration suggests that G.H.-R.I.H. has a direct action on the gastric parietal cell [23].
• Histamine acting on H2-receptor-associated adenylate cyclase stimulates cyclic AMP formation and consequently secretion of hydrochloric acid in oxyntic cells [24].
• In addition to this effect, prostaglandin endoperoxides may inhibit histamine-stimulated cyclic AMP formation in oxyntic cells [24].

Gene context of Parietal Cells, Gastric

• We find that CD63 is present also in tubulovesicular elements, the intracellular compartments that contain the H,K-ATPase in unstimulated gastric parietal cells [25].
• PALS1 specifies the localization of ezrin to the apical membrane of gastric parietal cells [26].
• In addition, we revealed that two Cdc42 regulators, IQGAP1 and IQGAP2, are present in gastric parietal cells [27].
• In rabbit gastric parietal cells, unlike Rab11a, Rab11b did not colocalize or coisolate with H(+)/K(+)-ATPase [28].
• Its effects are likely mediated by the induction of heparin-binding epidermal-like growth factor (HB-EGF), a member of the EGF family of growth factors that is expressed by gastric parietal cells [29].

Analytical, diagnostic and therapeutic context of Parietal Cells, Gastric

• Immunofluorescence labeling localized this exchanger exclusively to the basolateral membrane of gastric parietal cells, and functional studies in oocytes indicated that SLC26A7 is a DIDS-sensitive Cl(-)/HCO(3)(-) exchanger that is active in both acidic and alkaline pH(i) [30].
• Immunocytochemistry using anti-AQP4 antibodies showed strong AQP4 protein expression at the basolateral membrane of gastric parietal cells in wild-type (+/+) mice [31].
• The effects of compounds affecting gastric acid secretion were studied on the formation of inositol phosphates after prelabelling with [3H]-inositol in enriched gastric parietal cells of the rat, prepared by isopycnic centrifugation with Percoll [32].
• Patch-clamp techniques have been applied to characterize the channels in the basolateral membrane of resting (cimetidine-treated, nonacid secreting) oxyntic cells isolated from the gastric mucosa of Necturus maculosa [33].
• The presence of thyroglobulin antibody, rheumatoid factor, antinuclear factor or gastric parietal cell antibodies did not interfere in the microsomal antibody ELISA but some sera with mitochondrial antibody activity appeared to cause a non-specific effect [34].

References