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1
Content available remote

Impairment by allyl isothiocyanate of gastric epithelial wound repair through inhibition of ion transporters

100%
Hayashi S., Nakamura E., Kubo Y., Takahashi N., Yamaguchi A., Matsui H., Hagen S. J., Takeuchi K.
Journal of Physiology and Pharmacology
|
2008
|
tom 59
|
nr 4
691-706
Isothiocyanate is a transient receptor potential ankyrin 1 (TRPA1) agonist and also an inhibitor of ion transporters such as anion exchanger (AE) and Na+/HCO3- co-transporter (NBC). We examined the expression of TRPA1 and ion transporters in monolayers of the rat gastric epithelial cell line RGM1 and investigated the involvement of these factors in the inhibitory action of isothiocyanate on epithelial wound healing. After obtaining a confluent monolayer, a round artificial wound of constant size was induced in the center of the cell monolayer using a pencil-type mixer with a rotating silicon tip. Immediately after the wound induction, cells at the edge of the wound started to form lamellipodia, migrating towards the center of wound, and the cell-free area decreased with time. Addition of allyl isothiocyanate to standard buffer suppressed the recovery of the wound in a concentration-dependent manner without affecting the viability of the RGM1 cells. Icilin, another TRPA1 agonist, dose-dependently inhibited wound repair. Likewise, 4,4’-diisothio- cyanatostilbene-2,2’-disulfonic acid (DIDS), a stilbene compound containing an isothiocyanate group, also inhibited the recovery of epithelial wounds. In addition, the repair of epithelial wounds was suppressed when the cells were incubated in Na+, Cl- or HCO3- free buffer. The RGM1 cells expressed the mRNAs of AE2a and NBC1 but not TRPA1. These results suggested that isothiocyanate impairs the repair of epithelial wounds in RGM1 cells, probably through the inhibition of ion transporters such as AE2a and NBC1 and not the activation of the TRPA1 channel. It is assumed that the process of epithelial repair is associated with the regulation of cell volume and intracellular pH (pHi) by these ion transporters.
2

Proinflammatory cytokines and Helicobacter pylori stimulate C-C chemokine expression in gastric epithelial cells

100%
Terano A., Shimada T., Ohtsuka Y., Watanabe N., Hiraishi H.
Journal of Physiology and Pharmacology. Supplement
|
1997
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tom 48
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nr 1
3
Content available remote

Helicobacter pylori inhibits expression of heat shock protein 70 (HSP70) in human epithelial cell line. Importance of Cag A protein

100%
Targosz A., Pierzchalski P., Krawiec A., Szczyrk U., Brzozowski T., Konturek S. J., Pawlik W. W.
Journal of Physiology and Pharmacology
|
2006
|
tom 57
|
nr 2
Heat shock proteins (HSP) are crucial for the maintenance of cell integrity under normal cell growth and at pathophysiological conditions such as colonization of gastric mucosa by Helicobacter pylori (Hp). The effect of Hp on mRNA expression for HSP70 in the gastric epithelial cells in vitro has been little studied and remains inconclusive. In this study we attempted to determine the alterations in gene expression for HSP70 induced by two live strains of Hp in the epithelial MKN7 cells. The following Hp strains were employed; 1) Hp strain expressing cagA and vacA, and 2) cagA and vacA negative Hp strain without or with addition of exogenous recombinant protein CagA. MKN7 cells were incubated in a standard medium RPMI 1640 supplemented with 10% fetal bovine serum at 37°C with 5% CO2 and humidified atmosphere under basal condition or in a presence of Hp (1x109 CFU per dish) without or with the recombinant CagA (10 µg/ml of RPMI 1640 medium). After 3h, 24h and 48 h of incubation with Hp and in some experiments with the prolonged incubation time up to 72 h, the cells were harvested, the total cellular RNA was isolated and the expression of mRNA for HSP70 was determined by RT-PCR. The incubation of the MKN cells with CagA protein alone failed to affect significantly the expression of HSP70. In contrast, the strain Hp (cagA+, vacA+) inhibited in time-dependent manner the expression of mRNA for HSP70. When the MKN7 cells were coincubated with Hp (cagA+, vacA+) and exogenous CagA, the significant inhibition of the signal intensity for HSP70 mRNA was observed at 3 h and 24 h of incubation and these effects were followed by complete disappearance of the signal for HSP70 mRNA at 48 h. The incubation of MKN7 with Hp (cagA-, vacA-) also significantly attenuated the expression of HSP70 mRNA with the most pronounced inhibitory effect observed at 72 h of incubation with this Hp strain. Addition of the recombinant CagA to Hp (cagA-, vacA-) completely suppressed the expression of HSP70 at 48 h and 72 h after the end of incubation periods. We conclude that 1) both, Hp (cagA+, vacA+) and Hp (cagA-, vacA-) inhibit expression of HSP70 in MKN7 human gastric epithelial cells independently of the presence or absence of cagA gene, and that 2) recombinant CagA protein may exert biological activity in vitro via acceleration of inhibitory effect of Hp negative for Cag A and VacA on HSP70 expression in epithelial cells infected with this bacteria.
4
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Relationship between Vac A toxin and ammonia in Helicobacter pylori-induced apoptosis in human gastric epithelial cells

84%
Chiozzi V., Mazzini G., Oldani A., Sciullo A., Ventura U., Romano M., Boquet P., Ricci V.
Journal of Physiology and Pharmacology
|
2009
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tom 60
|
nr 3
23-30
VacA toxin is one of the most important virulence factors produced by H. pylori even though neither its role nor its action mechanisms are completely understood. First considered as a toxin inducing only cell vacuolation, VacA causes apoptosis of gastric epithelial cells by targeting mitochondria. A hotly debated question about VacA action is its relationship with ammonia, which is produced in vivo by H. pylori urease. While ammonia is strictly required for VacA-dependent vacuolation, its role in VacA-induced apoptosis is much less defined. This study was thus aimed to investigate the relationship between VacA toxin and ammonia in H. pylori-induced mitochondrial damage and apoptosis of human gastric epithelial cells in culture by means of flow cytometry. Our results show that, unlike cell vacuolation, in MKN 28 cells neither apoptosis nor dissipation of mitochondrial transmembrane potential induced by VacA require ammonia. Nevertheless, ammonia significantly potentiates both these VacA-induced effects, but independently of the swelling of VacA-containing endosomes (i.e., vacuolation). Our findings make unlikely the hypothesis that ammonia-dependent swelling and rupture of endosomal vesicles in which VacA is sequestered after cell internalization may allow the toxin to reach mitochondria and trigger apoptosis.
5
Content available remote

Glycoconjugates with NeuAc-NeuAc-Gal-Glc are more effective at preventing adhesion of Helicobacter pylori to gastric epithelial cells than glycoconjugates with NeuAc-Gal-Glc

84%
Hata Y., Murakami M., Okabe S.
Journal of Physiology and Pharmacology
|
2004
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tom 55
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nr 3
Helicobacter pylori (H. pylori) adheres to human gastric epithelial cells, eliciting various gastroduodenal diseases. Gangliosides play a critical role in bacterial adhesion to cell surfaces. The present study examined how residues of gangliosides are important for inhibition of adhesion of H. pylori to MKN-45 cells. We measured adhesion or detachment effects of gangliosides on the interaction between MKN-45 cells and H. pylori, as well as interleukin-8 production. Among the gangliosides, O-Ac-GD3, GT1b, GD1a, GD1b, GT1a, and GD3 had potent dose dependent inhibitory effects on adhesion of H. pylori to MKN-45 cells, interleukin-8 production, and vacuole formation induced by H. pylori toxin binding to Vero cells. GD3 also accelerated bacterial detachment of MKN-45 cells with adherent H. pylori in a dose dependent manner. Such results strongly suggest that the mechanism involved in the inhibition of H. pylori adhesion is mediated by the variations of the residues of the NeuAc-NeuAc-Gal-Glc chain of gangliosides. NeuAc-NeuAc-Gal-Glc exhibits a more inhibitory effect on adhesion than the NeuAc-Gal-Glc chain. Such gangioside and oligosaccrharide sequences appear to have therapeutic importance for prevention of H. pylori adhesion, as well as reduction of both inflammation and gastric mucosal injuries.
6
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Rebamipide attenuates nonsteroidal anti-inflammatory drugs (NSAID) induced lipid peroxidation by the manganese superoxide dismutase (MnSOD) overexpression in gastrointestinal epithelial cell

67%
Nagano Y., Matsui H., Shimokawa O., Hirayama A., Tamura M., Nakamura Y., Kaneko T., Rai K., Indo H. P., Majima H. J., Hyodo I.
Journal of Physiology and Pharmacology
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2012
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tom 63
|
nr 2
7
Content available remote

Salt is an oxidative stressor for gastric epithelial cells

67%
Tamura M., Matsui H., Nagano Y. N., Kaneko T., Indo H. P., Majima H. J., Hyodo I.
Journal of Physiology and Pharmacology
|
2013
|
tom 64
|
nr 1
8
Content available remote

15-deoxy-delta12,14-prostaglandin J2 suppresses RANTES expression by inhibiting NADPH oxidase activation in Helicobater pylori-infected gastric epithelial cells

67%
Cha B., Lim J. W., Kim K. H., Kim H.
Journal of Physiology and Pharmacology
|
2011
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tom 62
|
nr 2
Peroxisome proliferators-activated receptor-g (PPAR-g) is a ligand-activated transcription factor. 15 deoxy-12,14 prostaglandin J2 (15d-PGJ2) is a potent PPAR- ligand and acts as an anti-inflammatory agent via PPAR--dependent and independent mechanisms. Helicobacter pylori (H. pylori) induces gastric inflammation by inducing the activation of oxidant-sensitive transcription factor NF-B and cytokine expression in gastric epithelial cells. Since 15d-PGJ2 inhibits NF-B activation in various cells, it may suppress H. pylori-induced inflammatory signaling and cytokine expression in gastric epithelial cells. The present study aims to determined the effect of 15d-PGJ2 on the activation of inflammatory mediators Jak/Stat (Janus kinase/signal transducers and activators of transcription) and induction of cytokine RANTES in H. pylori-infected gastric epithelial AGS cells. Since NADPH oxidase is a candidate for the production of reactive oxygen species in H. pylori-infected gastric epithelial cells, we determined the effect of 15d-PGJ2 on the activation of NADPH oxdase. AGS cells were cultured in the presence of H. pylori treated with or without 15d-PGJ2. The activations of NADPH oxidase and Jak1/Stat3, the levels of H2O2 and RANTES in the medium, and DNA binding activity of Stat3 were assessed. A Jak/Stat3 specific inhibitor AG490 and an inhibitor of NADPH oxidase diphenyleneiodonium (DPI) were treated to determine the direct involvement of Jak/Stat and NADPH oxidase on the production of H2O2 and RANTES in H. pylori-infected cells. H. pylori induced the production of H2O2 and RANTES as well as the activations of NADPH oxidase and Jak1/Stat3, which were inhibited by the treatment of 15d-PGJ2. DPI suppressed H. pylori-induced alterations similar to 15d-PGJ2. However, AG490 had no effect on NADPH oxidase activation, but reduced the level of RANTES in the medium released from H. pylori-infected cells. Conclusion: NADPH oxidase activation is an upstream signaling of Jak1/Stat3 activation and induction of RANTES in H. pylori-infected AGS cells. 15d-PGJ2, inhibits the activations of NADPH oxidase and Jak1/Stat3 and RANTES expression, suggesting that 15d-PGJ2 may be beneficial for the treatment of H. pylori-induced gastric inflammation.
9
Content available remote

Beta-carotene inhibits Helicobacter pylori-induced expression of inducible nitric oxide synthase and cyclooxygenase-2 in human gastric epithelial AGS cells

67%
Jang S. H., Lim J. W., Kim H.
Journal of Physiology and Pharmacology. Supplement
|
2009
|
tom 60
|
nr 7
10
Content available remote

Nitric oxide-induced IL-8 expression is mediated by NF-kappaB and AP-1 in gastric epithelial AGS cells

67%
Seo J. Y., Ju J.-H., Lim J. W., Mukaida N., Kim H.
Journal of Physiology and Pharmacology. Supplement
|
2009
|
tom 60
|
nr 7
11
Content available remote

Influence of gastrin on the expression of cyclooxygenase-2, hepatocyte growth factor and apoptosis-related proteins in gastric epithelial cells

67%
Konturek P. C., Kania J., Kukharsky V., Ocker S., Hahn E. G., Konturek S. J.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
nr 1
Several studies have shown a link between gastrin and gastric cancer, both in humans and animals, especially infected with Helicobacter pylori (H. pylori). However, the exact role of hypergastrinemia in gastric carcinogenesis remains still undetermined. The aim of the present study was to evaluate the interaction between gastrin, cyclooxygenase-2 (COX-2), hepatocyte growth factor (HGF) and apoptosis-related proteins (Bax, Bcl-2, caspase-3, survivin) in cultured gastric epithelial cancer cells. Material and Methods: In the present study, gastric cultured cancer cells (KATO III cells) were exposed to increasing concentrations of gastrin (1-1000 nM). Cells incubated with culture medium alone, without added gastrin, served as controls. Using RT-PCR and Western blot, we examined the mRNA and protein expression for COX-2, HGF and apoptosis-related proteins (Bax, Bcl-2, caspase-3 and survivin). In addition, the gene expression of gastrin and gastrin receptor (CCK-2) as well as the release of gastrin in culture medium in the unstimulated cells were examined by RT-PCR and RIA, respectively. The apoptosis rate in cells was measured by flow cytometric analysis. Results: The present study shows that the gastric cultured epithelial cells exhibit the expression of gastrin and CCK-2 receptors and release of gastrin into the culture medium. The epithelial gastric cancer cells incubated with gastrin showed a concentration-dependent increase of COX-2 and HGF expression. Although no significant changes in apoptosis rate were observed, the exposure of these cells was associated with a dose-dependent increase in the expression of antiapoptotic proteins Bcl-2 and survivin. Conclusions: This study demonstrates that 1) gastrin stimulates the gene and protein expression of COX-2 and HGF in human cultured gastric cancer cells and 2) gastrin shows antiapoptotic activity through the upregulation of Bcl-2 and survivin.
12
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Content available

Helicobacter pylori stimulates gastric acid secretion via platelet activating factor

67%
Sobhani I., Bado A., Cherifi Y., Moizo L., Laigneau J. P., Pospai D., Mignon M., Lewin M. J.
Journal of Physiology and Pharmacology
|
1996
|
tom 47
|
nr 1
13
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Content available

Proinflammatory cytokines and Helicobacter pylori stimulate CC-chemokine expression in gastric epithelial cells

67%
Watanabe N., Shimada T., Ohtsuka Y., Hiraishi H., Terano A.
Journal of Physiology and Pharmacology
|
1997
|
tom 48
|
nr 3
14

The participation of ribosome-UDP-GalNAc complex in the initiation of protein glycosylation in vitro

67%
Paszkiewicz-Gadek A., Porowska H., Gindzienski A.
Acta Biochimica Polonica
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2000
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tom 47
|
nr 2
The gastric epithelial cells ribosome-UDP-GalNAc complex is a donor of UDP- GalNAc as the substrate for N-acetylgalactosaminyltransferase, which catalyse the transfer of GalNAc residue to the polypeptide, existing on polysomes. It was observed that the deglycosylated porcine mucin and synthetic peptide (PTSSPIST) can be also glycosylated with participation of N-acetylgalactosaminyltransferase and ribosome- UDP-GalNAc complex. The probability of the ribosome-UDP-GalNAc complex as an intermediate in the O-glycosylation is considered.
15
Content available remote

Role of heat shock proteins in gastric inflammation and ulcer healing

59%
Choi S. R., Lee S. A., Kim Y. J., Ok C. Y., Lee H. J., Hahm K. B.
Journal of Physiology and Pharmacology. Supplement
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2009
|
tom 60
|
nr 7
16
Content available remote

Alcoholic beverages and gastric epithelial cell viability: effect on oxidative stress-induced damage

59%
Loguercio C., Tuccillo C., Federico A., Fogliano V., Del Vecchio Blanco C., Romano M.
Journal of Physiology and Pharmacology. Supplement
|
2009
|
tom 60
|
nr 7
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