This site is intended for healthcare professionals
Journals
  • Home
  • /
  • Journals
  • /
  • Gastritis and duodenitis
  • /
  • Helicobacter pylori-induced chronic inflammation c...
Journal

Helicobacter pylori-induced chronic inflammation causes telomere shortening of gastric mucosa by promoting PARP-1-mediated non-homologous end joining of DNA.

Read time: 1 mins
Published:15th Sep 2016
Author: Lee WP, Hou MC, Lan KH, Li CP, Chao Y, Lin HC, et al.
Ref.:Arch Biochem Biophys. 2016 Sep 15;606:90-8.
DOI:10.1016/j.abb.2016.07.014. Epub 2016 Jul 19.
Helicobacter pylori-induced chronic inflammation causes telomere shortening of gastric mucosa by promoting PARP-1-mediated non-homologous end joining of DNA


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.

 

Read abstract on library site