Helicobacter pylori infection and gastric mucosal epithelial cell apoptosis

Olivares, David; Gisbert, Javier P.; Jm, Pajares García

doi:10.4321/s1130-01082005000700006

Cited by 13 publications

(8 citation statements)

References 125 publications

(130 reference statements)

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“…We dynamically observed the changes of apoptosis and proliferation of gastric mucosal cells at different times from 30 min to 6 h after gastric I/R injury, Histological study of the normal gastric mucosa revealed a few apoptotic cells in the superficial layer of gastric mucosa and proliferating cells only in the gastric glandular neck area. These patterns contrast with previous reports [43,44] , supporting the notion that cell renewal and apoptosis are two essential processes maintaining the homeostasis of normal gastric mucosa. The pattern of simultaneous change in gastric mucosal cellular apoptosis during reperfusion is similar to that of gastric I/R injury; i.e., the level of apoptosis also reached its peak at 1 h after reperfusion when the gastric mucosal injury was most serious, and then declined.…”

Section: Discussioncontrasting

confidence: 59%

Effects of hypothalamic paraventricular nuclei on apoptosis and proliferation of gastric mucosal cells induced by ischemia/reperfusion in rats

Zhang²,

Qiao³

et al. 2007

WJG

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Section: Discussioncontrasting

confidence: 59%

Effects of hypothalamic paraventricular nuclei on apoptosis and proliferation of gastric mucosal cells induced by ischemia/reperfusion in rats

Zhang²,

Qiao³

et al. 2007

WJG

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“…A histological study of the normal gastric mucosa showed a few apoptotic cells only in the superficial layer of the gastric mucosa and proliferative cells only in the gastric glandular neck area. These patterns contrast with previous reports, 34,35 supporting the notion that cell renewal and apoptosis are two essential processes maintaining the homeostasis of normal gastric mucosa. The pattern of changes with the time of gastric mucosal cellular apoptosis during reperfusion is similar to that of GI/RI (i.e.…”

Section: Discussionmentioning

confidence: 64%

Extracellular Signal‐regulated Kinase Pathways May Mediate the Protective Effect of Electrical Stimulation of the Paraventricular Nucleus Against Ischaemia–reperfusion Injury of the Gastric Mucosa

Zhang

Wei

et al. 2007

Clin Exp Pharma Physio

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1. The aim of the present study was to elucidate the role of the extracellular signal-regulated kinase (ERK) pathway in mediating the effects of electrical stimulation of the paraventricular nucleus (PVN) on apoptosis and proliferation induced by gastric ischaemia-reperfusion injury (GI/RI). 2. To investigate the effects of electrical stimulation of the hypothalamic PVN on gastric mucosal apoptosis and proliferation in response to ischaemia-reperfusion (I/R), we used a GI/RI model by clamping the coeliac artery for 30 min and then reperfusing the artery for 30 min or 1, 3 or 6 h. We used immunohistochemistry and western blotting to investigate the expression, activation and distribution of ERKs and the dynamic changes in their downstream cellular factors Bcl-2 and Bax at different times subsequent to electrical stimulation of the PVN in the I/R-injured gastric mucosa. 3. Electrical stimulation of the PVN markedly attenuated GI/RI at 30 min and 1 and 3 h after reperfusion. Electrical stimulation decreased gastric mucosal apoptosis, increased gastric mucosal proliferation and promoted the expression and activation of phosphorylated (p)-ERK1/2 30 min after reperfusion. Electrical stimulation increased the expression of Bcl-2 and decreased the expression of Bax at 30 min and 1 and 3 h after reperfusion. In contrast, inhibition of ERK1/2 activity by the specific upstream mitogen-activated protein kinase kinase inhibitor PD98059 produced similar effects at 1 h after reperfusion in rats subjected to I/R with or without electrical stimulation of the PVN. Administration of PD98059 aggravated gastric mucosal injury, increased apoptosis, decreased proliferation in gastric mucosal cells, decreased the expression and activity of p-ERK1/2 and Bcl-2 expression and increased Bax expression. 4. These results indicate that the PVN protects against GI/RI and that this protection is associated with the inhibition of cellular apoptosis and the promotion of proliferation in the gastric mucosa, probably by activating the ERK pathway.

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“…During lifelong infection in the hostile niche of the stomach, H. pylori seems to initiate the multi‐step process of carcinogenesis. Among various contributors in gastric carcinogenesis, H. pylori ‐initiated apoptosis of epithelial cells acts as a crucial pathogenic mechanism that stimulates rapid cellular proliferation as a compensatory event [26,27]. Induction of apoptosis is mainly dependent on the activation of executioner caspases that target several proteins such as cytoskeleton filaments, nuclear lamins, protein kinases, or other caspases as the substrates [28].…”

Section: Discussionmentioning

confidence: 99%

A Potential Association between Helicobacter pylori CagA EPIYA and Multimerization Motifs with Cytokeratin 18 Cleavage Rate during Early Apoptosis

et al. 2012

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Background and Aims: Helicobacter pylori is a highly diverse pathogen, which encounters epithelial cells as the initial defense barrier during its lifelong infection. The structure of epithelial cells can be disrupted through cleavage of microfilaments. Cytokeratin 18 (CK18) is an intermediate filament, the cleavage of which is considered an early event during apoptosis following activation of effector caspases. Methods: Helicobacter pylori strains were isolated from 76 dyspeptic patients. cagA 3’ variable region and CagA protein status were analyzed by PCR and western blotting, respectively. Eight hours post‐co‐culture of AGS cells with different H. pylori strains, flow cytometric analysis was performed using M30 monoclonal antibody specific to CK18 cleavage‐induced neo‐epitope. Results: Higher rates of CK18 cleavage were detected during co‐culture of AGS cells with H. pylori strains bearing greater numbers of cagA EPIYA‐C and multimerization (CM) motifs. On the other hand, H. pylori strains with greater numbers of EPIYA‐B relative to EPIYA‐C demonstrated a decrease in CK18 cleavage rate. Thus, H. pylori‐mediated cleavage of CK18 appeared proportional to the number of CagA EPIYA‐C and CM motifs, which seemed to be downplayed in the presence of EPIYA‐B motifs. Conclusions: Our observation associating the heterogeneity of cagA variants with the potential of H. pylori strains in the induction of CK18 cleavage as an early indication of apoptosis in gastric epithelial cells supports the fact that apoptosis may be a type‐specific trait. However, additional cagA‐targeted experiments are required to clearly identify the role of EPIYA and CM motifs in apoptosis and/or the responsible effector molecules.

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Helicobacter pylori infection and gastric mucosal epithelial cell apoptosis

Cited by 13 publications

References 125 publications

Effects of hypothalamic paraventricular nuclei on apoptosis and proliferation of gastric mucosal cells induced by ischemia/reperfusion in rats

Effects of hypothalamic paraventricular nuclei on apoptosis and proliferation of gastric mucosal cells induced by ischemia/reperfusion in rats

Extracellular Signal‐regulated Kinase Pathways May Mediate the Protective Effect of Electrical Stimulation of the Paraventricular Nucleus Against Ischaemia–reperfusion Injury of the Gastric Mucosa

A Potential Association between Helicobacter pylori CagA EPIYA and Multimerization Motifs with Cytokeratin 18 Cleavage Rate during Early Apoptosis

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