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 A redox-based mechanism for induction of interleukin-1 production by nitric oxide in a human colonic epithelial cell line (HT29-Cl.16E)

1996 ◽  
Vol 313 (1) ◽  
pp. 35-38 ◽  
Author(s):  
Geneviève VALLETTE ◽  
Anne JARRY ◽  
Jean-Eric BRANKA ◽  
Christian L. LABOISSE
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cell ◽  
Cell Line ◽  
Interleukin 1 ◽  
Epithelial Cell Line ◽  
Dependent Manner ◽  
Colonic Epithelial Cell ◽  
Colonic Epithelial Cell Line ◽  
Dose Dependent ◽  
Human Colonic Epithelial Cell

We evaluated the effects of two NO donors, sodium nitroprusside (SNP) and 3-morpholino-sydnonimine (SIN-1), characterized by alternative redox states, i.e. nitrosonium ion (NO+) and nitric oxide (NO•) respectively, on intracellular interleukin-1 (IL-1) production, by a human colonic epithelial cell line (HT29-Cl.16E). SNP was able to induce intracellular IL-1α production up to 10 h incubation, in a dose-dependent manner. Several experiments provide evidence that the NO+ redox form, and not the free radical NO•, is implicated in the IL-1α production: (i) SIN-1, devoid of any NO+ character, led to a very weak IL-1 production as compared with SNP; (ii) the reductive action of a thiol such as cysteine on NO+ led to a dose-dependent increase in NO• concentration, measured as NO2-/NO3- accumulation, and to a large decrease in IL-1 production. Dibutyryl cGMP had no effect on IL-1 production, this finding supporting the concept that a cGMP-independent pathway is involved in the intracellular signalling of NO+. Together these results point out that NO, depending on its redox form, is able to modulate IL-1 production in cultured colonic epithelial cells.

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.

scholarly journals Allyl Isothiocyanate Increases MRP1 Function and Expression in a Human Bronchial Epithelial Cell Line

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Dian-lei Wang ◽  
Chen-yin Wang ◽  
Yin Cao ◽  
Xian Zhang ◽  
Xiu-hua Tao ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Protein Expression ◽  
Cell Line ◽  
Allyl Isothiocyanate ◽  
Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Bronchial Epithelial ◽  
Mrp1 Protein

Multidrug resistance-associated protein 1 (MRP1), a member of the ATP-binding cassette (ABC) superfamily of transporters, plays an important role in normal lung physiology by protecting cells against oxidative stress and toxic xenobiotics. The present study investigates the effects of allyl isothiocyanate (AITC) onMRP1mRNA and MRP1 protein expression and transporter activity in the immortalised human bronchial epithelial cell line 16HBE14o-.MRP1mRNA and MRP1 protein expression in 16HBE14o- cells that were treated with allyl isothiocyanate were analysed by real-time PCR assay and Western blotting. The transport of carboxyfluorescein, a known MRP1 substrate, was measured by functional flow cytometry to evaluate MRP1 activity. Treatment with AITC at concentrations of 5–40 μM increased MRP1 protein levels in a concentration-dependent manner. AITC treatments at concentrations of 1–40 μM caused concentration-dependent increases inMRP1mRNA levels that were up to seven times greater than the levels found in control cells. Finally, AITC treatment at concentrations of 5–40 μM significantly increased MRP1-dependent efflux in 16HBE14o- cells. These results suggest that AITC can increase the expression and activity of MRP1 in 16HBE14o- cells in a concentration-dependent manner. The upregulation of MRP1 activity and expression by AITC could produce therapeutic effects in the treatment of lung disease.

Direct and indirect effects of H. pylori in cell cycle of gastric epithelial cell line AGS

1995 ◽  
Vol 108 (4) ◽  
pp. A92
Author(s):  
XG Fan ◽  
D Kelleher ◽  
XJ Fan ◽  
HX Xia ◽  
PWN Keeling
Keyword(s):  
Cell Cycle ◽  
Epithelial Cell ◽  
Cell Line ◽  
Indirect Effects ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Line ◽  
Direct And Indirect Effects ◽  
H Pylori

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
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