Highly histamine-responsive clones from the human gastric adenocarcinoma cell line HGT-1

Cheret, A.M.; Laboisse, Christian L.; Roumagnac, I.; Augeron, Chantal; Lewin, M. J. M.

doi:10.1007/bf01965510

Cited by 7 publications

(4 citation statements)

References 6 publications

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“…The fact that PAF production could be stimulated by Ca 2 further supports a central role of calcium in this production. However, the concentrations required for histamine and VIP to stimulate PAF production were much higher than those for stimulating cAMP (10 nmol L [16][17][18][19]. These findings are consistent with PAF production by the HGT1 cells being dependent on phospholipase A 2 (PLA 2 ) activation, as has been reported for canine kidney and lung epithelial cells [29,30].…”

Section: Discussionsupporting

confidence: 68%

“…These mediators are known to increase intracellular cAMP in these cells [19]. However, the concentrations required for histamine and VIP to stimulate PAF production were much higher than those for stimulating cAMP (10 nmol L [16][17][18][19]. Furthermore, our data clearly show that cAMP failed to enhance PAF production.…”

Section: Discussionmentioning

confidence: 64%

“…We and others have demonstrated that HGT1 cells display specific surface receptors for histamine, VIP and carbachol [17][18][19]. Several mediators have been shown to induce PAF synthesis from a variety of mononuclear or polynuclear cells, whereas histamine-and muscarinicmediated PAF production has been reported in mast cells [7,8].…”

Section: Discussionmentioning

confidence: 99%

“…Yet we and others have reported that PAF can be produced by intestinal mucosa whether or not the intestine is infiltrated by proinflammatory cells or not [15,16]; moreover, PAF synthesis in endothelial cells has been shown to be regulated by histamine and dopamine [6][7][8]. In this study, we have investigated in vitro production of PAF from gastric epithelial cells in response to histamine, VIP and carbachol using the human gastric tumour cell HGT1-clone 6 as a model [17][18][19][20].…”

Section: Introductionmentioning

confidence: 99%

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Regulation of platelet‐activating factor production in gastric epithelial cells

Sobhani

Denizot

Moizo

et al. 1996

Eur J Clin Investigation

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The authors have previously reported that platelet-activating factor (PAF), a phospholipid mediator with potent proinflammatory activities, is produced in the gastric mucosa and stimulates gastric acid secretion in humans and animals. In the present study they used the human gastric tumour cells HGT1 (clone 6) to examine whether PAF production is regulated by neuromediators. PAF was extracted by ethanol and assayed by the washed platelet aggregation test. HGT1 cells produced PAF spontaneously (110 +/- 20 pg 10(6) cells). The addition of vasoactive intestinal peptide (VIP; 10(-9) to 10(-7) mol L(-1)) or of histamine (10(-5) to 10(-3) mol L(-1)) increased PAF production by three- to fivefold, while the addition of carbachol (10(-7) to 10(-4) mol L(-1)) increased PAF production up to sevenfold. PAF production was also increased up to 10- to 13-fold, in a dose- and time-dependent manner, by the addition of calcium and two- to threefold by the addition of phorbol myristate acetate (PMA; 10(-7) to 10(-5) mol L(-1)). However, the addition of dibutyryl cyclic AMP (dBcAMP; 10(-6) to 10(-4) mol L(-1) was without any effect. This is the first report showing PAF production by gastric epithelial cells in response to histamine, VIP and carbachol. Furthermore, the findings are consistent with a central role of calcium in this production. The results of this study, together with those of previous studies from the authors' laboratory, support the hypothesis that PAF is a physiological mediator of gastric acid secretion.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Regulation of platelet‐activating factor production in gastric epithelial cells

Sobhani

Denizot

Moizo

et al. 1996

Eur J Clin Investigation

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A cAMP-activated chloride channel in the plasma membrane of cultured human gastric cells (HGT-1)

et al. 1990

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Hydrochloric acid (HCl) secretion by gastric parietal cells involves an apical Cl- conductance, the properties of which have not been defined. In the present study, forskolin and histamine [agonists that increase intracellular cyclic adenosine monophosphate (cAMP)], and dibutyryl cAMP, activated channels in previously quiescent cell-attached membrane patches on cultured human gastric cells (HGT-1). In the cell-attached configuration (Cl- 149 mmol/l in bath and pipette), channels exhibited outward rectification, voltage dependence, inward current (-0.7 pA) at zero holding potential and a reversal potential of +24 mV, consistent with the presence of a Cl- conductive pathway. In excised inside-out patches, channels (i) exhibited degrees of outward rectification and voltage dependence that were comparable to those seen in cell-attached patches, (ii) demonstrated a -21 mV shift of their reversal potential when bath Cl- was decreased from 149 mmol/l to 53 mmol/l (calculated Cl-:cation permeability ratio 17:1), and (iii) were highly sensitive to the Cl- channel blocker diphenylamine-2-carboxylic acid (DPC, 10(-3) mol/l). This cAMP-activated Cl- channel bears many similarities to other Cl- channels within intestinal epithelia, and may represent the apical Cl- channel operating in HCl-secreting gastric parietal cells.

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Molecular characterization of a purified human gastric somatostatin receptor

Lewin

Reyl-Desmars

1990

Metabolism

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Highly histamine-responsive clones from the human gastric adenocarcinoma cell line HGT-1

Cited by 7 publications

References 6 publications

Regulation of platelet‐activating factor production in gastric epithelial cells

Regulation of platelet‐activating factor production in gastric epithelial cells

A cAMP-activated chloride channel in the plasma membrane of cultured human gastric cells (HGT-1)

Molecular characterization of a purified human gastric somatostatin receptor

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