Role of Cytokines in Helicobacter pylori-Induced Gastric Epithelial Cell Matrix Metalloproteinase Secretion and Activation

2002 ◽  
pp. 123-126
Author(s):  
Monika Gööz ◽  
Maria Shaker ◽  
Pal Gööz ◽  
Adam J. Smolka
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cell ◽  
Matrix Metalloproteinase ◽  
Gastric Epithelial Cell ◽  
Cell Matrix

Regulation of gastric epithelial cell growth by Helicobacter pylori: Offdence for a major role of apoptosis

1997 ◽  
Vol 113 (6) ◽  
pp. 1836-1847 ◽  
Author(s):  
S Wagner ◽  
W Beil ◽  
J Westermann ◽  
RP Logan ◽  
CT Bock ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Cell Growth ◽  
Epithelial Cell ◽  
Gastric Epithelial Cell

scholarly journals The Role of Heat Shock Protein 60 (HSP60) of Helicobacter pylori in Adhesion of H. pylori to Human Gastric Epithelial Cell

1998 ◽  
Vol 72 (5) ◽  
pp. 487-492 ◽  
Author(s):  
Hiroyuki YAMAGUCHI ◽  
Takako OSAKI ◽  
Naoto KURIHARA ◽  
Haruhiko TAGUCHI ◽  
Shigeru KAMIYA
Keyword(s):  
Helicobacter Pylori ◽  
Heat Shock ◽  
Epithelial Cell ◽  
Heat Shock Protein ◽  
Gastric Epithelial Cell ◽  
Heat Shock Protein 60 ◽  
H Pylori

The Role of Matrix Metalloproteinase-7 in Redefining the Gastric Microenvironment in Response to Helicobacter pylori

2006 ◽  
Vol 130 (6) ◽  
pp. 1754-1763 ◽  
Author(s):  
Catherine McCaig ◽  
Cedric Duval ◽  
Elaine Hemers ◽  
Islay Steele ◽  
D. Mark Pritchard ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 7

scholarly journals Helicobacter pylori cagA+ Strains and Dissociation of Gastric Epithelial Cell Proliferation From Apoptosis

1997 ◽  
Vol 89 (12) ◽  
pp. 863-868 ◽  
Author(s):  
R. M. Peek ◽  
S. F. Moss ◽  
S. Wang ◽  
P. R. Holt ◽  
K. T. Tham ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Helicobacter Pylori ◽  
Epithelial Cell ◽  
Gastric Epithelial Cell ◽  
Epithelial Cell Proliferation

Tu1196 EFFECT OF HELICOBACTER PYLORI ON THE JUNCTIONAL PROTEIN EXPRESSIONS IN THE NORMAL HUMAN GASTRIC EPITHELIAL CELL DERIVED FROM GASTRIC ORGANOID IN VITRO.

2020 ◽  
Vol 158 (6) ◽  
pp. S-1014-S-1015
Author(s):  
Byeong Min Yu ◽  
Yong Chan Lee ◽  
CHANG Y. JUNG ◽  
So Dam Lee ◽  
Bo Ram Hwang ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cell ◽  
Gastric Epithelial Cell ◽  
Protein Expressions ◽  
Junctional Protein ◽  
Normal Human

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.

Modification of Ganglioside Content of Human Gastric Epithelial Cell Membrane Decreases Helicobacter pylori Adhesion

2017 ◽  
Vol 65 (4) ◽  
pp. 456-461 ◽  
Author(s):  
Irma Magaly Rivas-Serna ◽  
Vera C. Mazurak ◽  
Monika Keelan ◽  
Michael Thomas Clandinin
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cell ◽  
Cell Membrane ◽  
Gastric Epithelial Cell ◽  
Ganglioside Content
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