Phospholipase A 2 stimulates rat gastric epithelial cell line (RGM-1) migration

1997 ◽  
Vol 46 (3) ◽  
pp. 103-107 ◽  
Author(s):  
T. Minami ◽  
H. Tojo ◽  
S. Zushi ◽  
Y. Shinomura ◽  
Y. Matsuzawa
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Gastric Epithelial Cell ◽  
Phospholipase A ◽  
Epithelial Cell Line ◽  
Phospholipase A 2

HGF regulates tight junctions in new nontumorigenic gastric epithelial cell line

2001 ◽  
Vol 280 (5) ◽  
pp. G910-G921 ◽  
Author(s):  
Frederic Hollande ◽  
Emmanuelle M. Blanc ◽  
Jean Pierre Bali ◽  
Robert H. Whitehead ◽  
Andre Pelegrin ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cell ◽  
Tight Junction ◽  
Cell Line ◽  
Cell Monolayer ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line ◽  
Dependent Manner ◽  
Membrane Expression ◽  
Epithelial Cell Differentiation

The regulation of intercellular adhesion by hepatocyte growth factor (HGF) was examined on a novel nontumorigenic gastric epithelial cell line (IMGE-5) derived from H-2Kb-tsA58 transgenic mice. IMGE-5 cells constitutively expressed cytokeratin 18 and HGF receptors. Under permissive conditions (33°C + interferon-γ), IMGE-5 cells proliferated rapidly but did not display membrane expression of adherens and tight junction proteins. Under nonpermissive conditions, their proliferation was decreased and they displayed a strong, localized membrane expression of E-cadherin/β-catenin and occludin/ZO-1. HGF treatment largely prevented the targeting of ZO-1 to the tight junction and induced a significant decrease of the transepithelial resistance measured across a confluent IMGE-5 cell monolayer. HGF rapidly increased the tyrosine phosphorylation of ZO-1 and decreased its association with occludin in a phosphatidylinositol 3-kinase (PI 3-kinase)-dependent manner. PI 3-kinase was also involved in HGF-induced migration of IMGE-5 cells. Our results demonstrate that 1) HGF prevents the appearance of ZO-1 in the membrane during epithelial cell differentiation; 2) HGF causes partial relocalization of ZO-1 to the cytoplasm and nucleus and concomitantly stimulates cell dissociation and migration; and 3) IMGE-5 cells offer a useful model for the study of gastric epithelial cell differentiation.

scholarly journals Rapid Interaction ofHelicobacter pyloriwith Microvilli of the Polar Human Gastric Epithelial Cell Line NCI-N87

2013 ◽  
Vol 296 (12) ◽  
pp. C1-C1
Author(s):  
Anne-Kathrin Diesing ◽  
Constanze Nossol ◽  
Heidi Faber-Zuschratter ◽  
Werner Zuschratter ◽  
Lydia Renner ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line

scholarly journals Effect of Astaxanthin on Activation of Autophagy and Inhibition of Apoptosis in Helicobacter pylori-Infected Gastric Epithelial Cell Line AGS

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1750 ◽  
Author(s):  
Hanbit Lee ◽  
Joo Weon Lim ◽  
Hyeyoung Kim
Keyword(s):  
Helicobacter Pylori ◽  
Protein Kinase ◽  
Epithelial Cell ◽  
Cell Line ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line ◽  
Ags Cells ◽  
Compound C ◽  
H Pylori ◽  
Induced Apoptosis

Helicobacter pylori (H. pylori) infection leads to the massive apoptosis of the gastric epithelial cells, causing gastric ulcers, gastritis, and gastric adenocarcinoma. Autophagy is a cellular recycling process that plays important roles in cell death decisions and can protect cells by preventing apoptosis. Upon the induction of autophagy, the level of the autophagy substrate p62 is reduced and the autophagy-related ratio of microtubule-associated proteins 1A/1B light chain 3B (LC3B)-II/LC3B-I is heightened. AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) are involved in the regulation of autophagy. Astaxanthin (AST) is a potent anti-oxidant that plays anti-inflammatory and anti-cancer roles in various cells. In the present study, we examined whether AST inhibits H. pylori-induced apoptosis through AMPK-mediated autophagy in the human gastric epithelial cell line AGS (adenocarcinoma gastric) in vitro. In this study, H. pylori induced apoptosis. Compound C, an AMPK inhibitor, enhanced the H. pylori-induced apoptosis of AGS cells. In contrast, metformin, an AMPK activator, suppressed H. pylori-induced apoptosis, showing that AMPK activation inhibits H. pylori-induced apoptosis. AST inhibited H. pylori-induced apoptosis by increasing the phosphorylation of AMPK and decreasing the phosphorylation of RAC-alpha serine/threonine-protein kinase (Akt) and mTOR in H. pylori-stimulated cells. The number of LC3B puncta in H. pylori-stimulated cells increased with AST. These results suggest that AST suppresses the H. pylori-induced apoptosis of AGS cells by inducing autophagy through the activation of AMPK and the downregulation of its downstream target, mTOR. In conclusion, AST may inhibit gastric diseases associated with H. pylori infection by increasing autophagy through the activation of the AMPK pathway.

CHARACTERIZATION OF JOK-1, A HUMAN GASTRIC EPITHELIAL CELL LINE

2000 ◽  
Vol 36 (4) ◽  
pp. 228-234
Author(s):  
N. OKAYAMA ◽  
M. R. FOWLER ◽  
S. R. JENNINGS ◽  
P. PATEL ◽  
R. SPECIAN ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line

The mongolian gerbil gastric epithelial cell line immortalized by SV-40 large T antigen

2001 ◽  
Vol 120 (5) ◽  
pp. A745-A746
Author(s):  
K YOSHIURA ◽  
T SHIMADA ◽  
T MITSUHASHI ◽  
K TAKAHASHI ◽  
H HIRAISHI ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Mongolian Gerbil ◽  
T Antigen ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line ◽  
Large T Antigen

CHARACTERIZATION OF JOK-1, A HUMAN GASTRIC EPITHELIAL CELL LINE

2000 ◽  
Vol 36 (4) ◽  
pp. 228 ◽  
Author(s):  
N. OKAYAMA ◽  
M. R. FOWLER ◽  
S. R. JENNINGS ◽  
P. PATEL ◽  
R. SPECIAN ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line
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