Uptake and methylation of histamine by dispersed gastric mucosal cells and its possible influence on acid secretion

1990 ◽  
Vol 68 (1) ◽  
pp. 71-78 ◽  
Author(s):  
A. Wollin
Keyword(s):  
Target Cells ◽  
Gastric Mucosal Cells ◽  
Histamine Concentration ◽  
Mucosal Cells ◽  
Histamine Uptake ◽  
Independent Process ◽  
Methylation Activity ◽  
Product Accumulation ◽  
Uptake And Metabolism ◽  
Histamine Methylation

Inactivation of histamine by gastric mucosal tissue was examined in dispersed rabbit gastric mucosal cells. Mucosal cells were incubated with [14C]histamine. The formed radioactive metabolites were separated and identified by thin layer co-chromatography and quantitated, in both the cellular and extracellular mediums. Gastric mucosal cells internalized histamine, most of which was immediately methylated primarily to Nτ-methylhistamine and released. Cellular histamine product accumulation reached a plateau. The rate of histamine methylation increased with increasing extracellular histamine concentration, moving towards a plateau above 5 μM. Histamine methylation was greatly decreased but not abolished at 4 °C, in the absence of Na+ and by phlorizin (0.5 mM), an inhibitor of Na+-dependent co-transport. Inhibition of histamine N-methyltransferase decreased intracellular methylhistamine content dose dependently without increasing intracellular histamine. The secretagogues pentagastrin and carbachol did not influence histamine metabolism but ethanol inhibited methylation. The data suggest that gastric mucosal cells take up histamine by a Na+-dependent and Na+-independent process. The histamine uptake capacity appears to be linked to the methylation activity within the cell. The decrease in histamine uptake and metabolism caused by ethanol could potentially increase histamine concentrations near the target cells and be the reason for the stimulatory effect of ethanol on acid secretion.Key words: rabbit mucosa, histamine uptake, histamine N-methyltransferase, Nτ-methylhistamine, ethanol.

In vitro Action of Gastric Mucosal Lysosomal Enzymes on Intracellular Gastric Glycoproteins

1979 ◽  
Vol 34 (1-2) ◽  
pp. 90-95 ◽  
Author(s):  
Fouad M. Fouad ◽  
D. Waldron-Edward
Keyword(s):  
Cell Wall ◽  
Lysosomal Enzymes ◽  
Gastric Ulceration ◽  
Mucosal Cell ◽  
Gastric Lesions ◽  
Acid Hydrolases ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells ◽  
Specific Increase

Abstract The results show that incubation of gastric mucosal cells from rat at pH ~4.5 or in the presence of aspirin is associated with a specific increase in the activity of some acid-hydrolases. Intracellular glycoproteins, isolated by non-degradative techniques from rat or dog fundic mucosal cells, were found to be potential bio-substrates for these acid-hydrolyses. This may suggest that cleavage of the carbohydrate moieties of the intracellular and mucosal cell wall glycoproteins is a fundamental step in the development of gastric ulceration. A model for gastric lesions is proposed and discussed in the light of the results obtained.

Establishment of primary epithelial cell culture from elutriated rat gastric mucosal cells

1995 ◽  
Vol 30 (2) ◽  
pp. 135-141 ◽  
Author(s):  
Yoshikazu Kinoshita ◽  
Sazzad Hassan ◽  
Hirohisa Nakata ◽  
Masakyo Asahara ◽  
Yumi Matsushima ◽  
...  
Keyword(s):  
Cell Culture ◽  
Epithelial Cell ◽  
Epithelial Cell Culture ◽  
Gastric Mucosal Cells ◽  
Primary Epithelial Cell ◽  
Mucosal Cells

Evidence for direct cellular protective effect of PL-10 substances (synthesized parts of body protection compound, BPC) and their specificity to gastric mucosal cells

Life Sciences ◽  
1997 ◽  
Vol 61 (16) ◽  
pp. PL243-PL248 ◽  
Author(s):  
Beáta Bódis ◽  
Oszkár Karádi ◽  
Péter Németh ◽  
Csaba Dohoczky ◽  
Marko Kolega ◽  
...  
Keyword(s):  
Protective Effect ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells

scholarly journals Major Histocompatibility Complex Class II Inhibits Fas Antigen-Mediated Gastric Mucosal Cell Apoptosis through Actin-Dependent Inhibition of Receptor Aggregation

2005 ◽  
Vol 73 (10) ◽  
pp. 6311-6321 ◽  
Author(s):  
Calin Stoicov ◽  
Xun Cai ◽  
Hanchen Li ◽  
Kristine Klucevsek ◽  
Jane Carlson ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Mucosal Cell ◽  
Complex Class ◽  
Gastric Mucosal Cells ◽  
Fas Antigen ◽  
Histocompatibility Complex ◽  
Receptor Aggregation ◽  
Mucosal Cells

ABSTRACT Escape from normal apoptotic controls is thought to be essential for the development of cancer. During Helicobacter pylori infection, the leading cause of gastric cancer, activation of the Fas antigen (Fas Ag) apoptotic pathway is responsible for early atrophy and tissue loss. As disease progresses, metaplastic and dysplastic glands arise which express Fas Ag but are resistant to apoptosis and are believed to be the precursor cells for adenocarcinoma. In this report, we show that one mechanism of acquired Fas resistance is inhibition of receptor aggregation via a major histocompatibility complex class II (MHCII)-mediated, actin-dependent mechanism. For these studies we used the well-described C57BL/6 mouse model of Helicobacter pylori and Helicobacter felis infection. Under normal conditions, Fas Ag is expressed at low levels, and MHCII expression on gastric mucosal cells is negligible. With infection and inflammation, both receptors are upregulated, and 6.1% of gastric mucosal cells express MHCII in combination with Fas Ag. Using the rat gastric mucosal cell line RGM-1 transfected with murine Fas Ag and MHCIIαβ chains, we demonstrate that MHCII prevents Fas receptor aggregation and inhibits Fas-mediated signaling through its effects on the actin cytoskeleton. Depolymerization of actin with cytochalasin D allows receptors to aggregate and restores Fas sensitivity. These findings offer one mechanism by which gastric mucosal cells acquire Fas resistance.

Muscarinic M2-receptors enhance polyphosphoinositol release in rat gastric mucosal cells

FEBS Letters ◽  
1986 ◽  
Vol 204 (2) ◽  
pp. 352-356 ◽  
Author(s):  
Andreas Pfeiffer ◽  
Gustav Paumgartner ◽  
Albert Herz
Keyword(s):  
Gastric Mucosal Cells ◽  
Mucosal Cells ◽  
Muscarinic M2 Receptors
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