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• W2112464720 abstract "<b>Background:</b> Although activation of mitogen activated protein kinases (MAPKs) by <i>Helicobacter pylori</i> infection is associated with induction of host angiogenesis, which may contribute to <i>H pylori</i> associated gastric carcinogenesis, the strategy for its prevention has not been identified. As we previously reported a strong inhibitory action of gastric proton pump inhibitors (PPIs) on MAPK extracellular signal regulated kinase (ERK)1/2 phosphorylation, we investigated whether PPIs could suppress the <i>H pylori</i> induced angiogenesis via inhibition of MAPK ERK1/2. <b>Methods:</b> To address the relationship between <i>H pylori</i> infection and angiogenesis, comparative analysis of density of CD34⁺ blood vessel was performed in tissues obtained from 20 <i>H pylori</i> positive gastritis and 18 <i>H pylori</i> negative gastritis patients. Expression of hypoxia inducible factor 1 (HIF-1α) and vascular endothelial growth factor (VEGF) was tested by reverse transcription-polymerase chain reaction and secretion of interleukin 8, and VEGF was measured by ELISA. To evaluate the direct effect of <i>H pylori</i> infection on the tubular formation of human umbilical vein endothelial cells (HUVEC), an in vitro angiogenesis assay was employed. Activation of MAPK and nuclear factor κB (NFκB) was detected by immunoblotting. <b>Results:</b><i>H pylori</i> positive gastritis patients showed a higher density of CD34⁺ blood vessels (mean 40.9 (SEM 4.4)) than <i>H pylori</i> negative gastritis patients (7.2±0.8), which was well correlated with expression of HIF-1α. Conditioned media from <i>H pylori</i> infected gastric epithelial cells directly induced tubular formation of HUVEC and the increase of in vitro angiogenesis was suppressed by PPI treatment. Infection of <i>H pylori</i> significantly upregulated expression of HIF-1α and VEGF in gastric epithelial cells and expression of proangiogenic factors was mediated by MAPK activation and partially responsible for NFκB activation. PPIs effectively inhibited the phosphorylation of MAPK ERK1/2 that is a principal signal for <i>H pylori</i> induced angiogenesis. <b>Conclusions:</b> The fact that PPIs could downregulate <i>H pylori</i> induced angiogenesis indicates that antiangiogenic treatment using a PPI could be a promising protective therapeutic approach for <i>H pylori</i> associated carcinogenesis." @default.
• W2112464720 created "2016-06-24" @default.
• W2112464720 creator A5080005020 @default.
• W2112464720 date "2006-01-01" @default.
• W2112464720 modified "2023-10-16" @default.
• W2112464720 title "Novel action of gastric proton pump inhibitor on suppression of Helicobacter pylori induced angiogenesis" @default.
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• W2112464720 doi "https://doi.org/10.1136/gut.2005.067454" @default.
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