scholarly journals Intrinsic factor: active and inhibitory components from the mitochondria of human gastric mucosal cells

1961 ◽  
Vol 80 (2) ◽  
pp. 342-348 ◽  
Author(s):  
WH TAYLOR ◽  
BJ MALLETT ◽  
KB TAYLOR
Keyword(s):  
Intrinsic Factor ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells ◽  
Inhibitory Components

Intrinsic factor secretion from isolated human gastric mucosal cells

1984 ◽  
Vol 804 (2) ◽  
pp. 192-199 ◽  
Author(s):  
Wolfgang Schepp ◽  
Siegfried Ernst Miederer ◽  
Hans-Jörg Ruoff
Keyword(s):  
Intrinsic Factor ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells ◽  
Factor Secretion

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.

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