Suppression of Helicobacter pylori-induced Angiogenesis by a Gastric Proton Pump Inhibitor.
10.5230/jkgca.2005.5.3.191
- Author:
Sung Ho JIN
1
;
Hwa Young LEE
;
Dong Kyu KIM
;
Yong Kwan CHO
;
Ki Baik HAHM
;
Sang Uk HAN
Author Information
1. Department of Surgery, Ajou University School of Medicine, Suwon, Korea. hansu@ajou.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Helicobacter pylori;
Gastric cancer;
Carcinogenesis;
Angiogenesis;
Proton pump inhibitor
- MeSH:
Blood Vessels;
Carcinogenesis;
Culture Media, Conditioned;
Gastric Mucosa;
Gastritis;
Helicobacter pylori;
Helicobacter*;
Human Umbilical Vein Endothelial Cells;
Humans;
Phosphorylation;
Phosphotransferases;
Proton Pumps*;
Protons*;
Stomach Neoplasms;
Vascular Endothelial Growth Factor A
- From:Journal of the Korean Gastric Cancer Association
2005;5(3):191-199
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Though infections of Helicobacter pylori (H. pylori) are closely associated with activation of host angiogenesis, the underlying mechanisms, as well as the strategy for its prevention, have not been identified. Here, we investigated a causal role of H. pylori infection in angiogenesis of gastric mucosa and a potent inhibitory effect of a gastric proton pump inhibitor (PPI) on the gastropathy. MATERIALS AND METHODS: A comparative analysis of CD 34 expression in tissues obtained from 20 H. pylori-associated gastritis and 18 H. pylori-negative gastritis patients was performed. Expression of HIF-1alpha and VEGF were tested by using RT-PCR. To evaluate the direct effect of H. pylori infection on differentiation of endothelial HUVEC cells, we carried out an in vitro angiogenesis assay. RESULTS: H. pylori-associated gastritis tissues showed significantly higher density of CD34+ blood vessels than did H. pylori-negative gastritis tissues, and the levels were well correlated with expressions of HIF-1alpha. Conditioned media from H. pylori-infected gastric mucosal cells stimulated a tubular formation of HUVEC cells. We also found a significant inhibitory effect of PPI, an agent frequently used for H. pylori eradication, on H. pylori-induced angiogenesis. This drug effectively inhibited the phosphorylation of MAP kinase ERK1/2, which is a principal signal for H. pylori-induced angiogenesis. CONCLUSION: The fact that PPIs can down-regulate H. pylori-induced angiogenesis suggest that anti-angiogenic treatment using PPI may be a preventive approach for H. pylori-associated carcinogenesis.
