幽门螺杆菌
端粒
胃粘膜
炎症
胃炎
癌症
慢性胃炎
DNA损伤
螺杆菌
萎缩性胃炎
生物
免疫学
胃
医学
胃肠病学
内科学
DNA
遗传学
作者
Wei‐Ping Lee,Ming‐Chih Hou,Keng‐Hsin Lan,Chung‐Pin Li,Yee Chao,Han-Chieh Lin,Shou‐Dong Lee
标识
DOI:10.1016/j.abb.2016.07.014
摘要
Helicobacter pylori infection leads to chronic gastritis and increased risk of gastric cancer. The mechanism involves chronic inflammation. We aimed to determine the mechanism by which H. pylori infection causes telomere shortening in inflammatory gastric mucosa. Gastric biopsy specimens were obtained from 20 patients with chronic gastritis or peptic ulcer caused by H. pylori infection. The specimens showed increased NF-κB and superoxide dismutase activities and elevated expressions of PARP-1 and γ-H2AX, all of which returned to normal levels after anti-H. pylori treatment, suggesting that oxidative DNA damage and PARP-1 overexpression might cause telomere shortening. In this report, we adopted DNA end joining assay and showed that H. pylori-infected gastric mucosa had increased alternative NHEJ (non-homologous end joining), implicating that telomere shortening was caused by inflammation-mediated overproduction of reactive oxygen species and PARP-1, leading to telomere shortening.
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