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Titolo:
Helicobacter pylori induces apoptosis in human epithelial gastric cells bystress activated protein kinase pathway
Autore:
Domek, MJ; Netzer, P; Prins, B; Nguyen, T; Liang, D; Wyle, FA; Warner, A;
Indirizzi:
Vet Affairs Med Ctr, Long Beach, CA USA Vet Affairs Med Ctr Long Beach CAUSA ffairs Med Ctr, Long Beach, CA USA Univ Calif Irvine, Irvine, CA USA Univ Calif Irvine Irvine CA USAUniv Calif Irvine, Irvine, CA USA
Titolo Testata:
HELICOBACTER
fascicolo: 2, volume: 6, anno: 2001,
pagine: 110 - 115
SICI:
1083-4389(2001)6:2<110:HPIAIH>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
N-TERMINAL KINASE; C-JUN; DNA-DAMAGE; PROLIFERATION; INDUCTION; ERADICATION; EXPRESSION; INFECTION; DEATH; ADHERENCE;
Keywords:
Helicobacter pylori; apoptosis; stress activated protein kinase; SAPK/JNK; cell growth inhibitor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Netzer, P Univ Bern, Inselspital, Gastrointestinal Unit, CH-3010 Bern, Switzerland Univ Bern Bern Switzerland CH-3010 , CH-3010 Bern, Switzerland
Citazione:
M.J. Domek et al., "Helicobacter pylori induces apoptosis in human epithelial gastric cells bystress activated protein kinase pathway", HELICOBACT, 6(2), 2001, pp. 110-115

Abstract

Background. The pathway by which Helicobacter pylori induces apoptosis in gastric epithelial cells is not known. The aim of this study was to determine whether H. pylori-induced apoptosis is associated with SAPK/JNK activityin human gastric cancer KATO III cells. Materials and Methods. H. pylori VacA toxin positive strain was incubated with KATO III cells for 0.5, 1, 2 or 24 hours. The SAPK/JNK protein was harvested from the KATO III cell lysate by precipitation with a C-jun fusion protein and Its activity was measured by C-jun phosphorylation utilizing transblotting and phosphoserine antibody. Cellular apoptosis was demonstrated by DNA fragmentation. In addition, cell growth in coculture with H. pylori was determined over 72 hours. Results. H. pylori significantly stimulated SAPK/JNK activity in KATO III cells with a peak at the 0.5 hour time point (3.6-fold vs. control, p <.05), but a return to basal levels by 2 hours. In addition, significant DNA fragmentation was observed after 24 hours in these cells but not in the control KATO III cells. Cell growth was inhibited in a dose dependent fashion in coculture with H. pylori. Conclusion. These results show that H. pylori triggers an increase in apoptosis in KATO III cells as reflected by DNA fragmentation. This effect was preceded and correlated with an increase in SAPK/JNK activity suggesting that the H. pylori-induced apoptosis in human gastric epithelial cells may bemediated by the SAPK/JNK pathway.

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Documento generato il 02/04/20 alle ore 21:53:52