Telomere length in non-neoplastic gastric mucosa and its relationship to H. pylori infection, degree of gastritis, and NSAID use

Tomomitsu Tahara, Tomoyuki Shibata, Tomohiko Kawamura, Takamitsu Ishizuka, Masaaki Okubo, Mitsuo Nagasaka, Yoshihito Nakagawa, Tomiyasu Arisawa, Naoki Ohmiya, Ichiro Hirata

研究成果: Article査読

11 被引用数 (Scopus)

抄録

Telomere shortening occurs with human aging in many organs and tissues and is accelerated by rapid cell turnover and oxidative injury. We measured average telomere length using quantitative real-time PCR in non-neoplastic gastric mucosa and assessed its relationship to H. pylori-related gastritis, DNA methylation, ulcer disease, and nonsteroidal anti-inflammatory drug (NSAID) usage. Gastric biopsies were obtained from 151 cancer-free subjects including 49 chronic NSAID users and 102 nonusers. Relative telomere length in genomic DNA was measured by real-time PCR. H. pylori infection status, histological severity of gastritis, and serum pepsinogens (PGs) were also investigated. E-cadherin (CDH1) methylation status was determined by methylation-specific PCR (MSP). Average relative telomere length of H. pylori-infected subjects was significantly shortened when compared to H. pylori-negative subjects (p = 0.002) and was closely associated with all histological parameter of gastritis (all p values <0.01) and CDH1 methylation (p = 0.0002). In H. pylori-negative subjects, NSAID users presented significantly shorter telomere length than nonusers (p = 0.028). Shorter telomere length was observed in duodenal and gastric ulcer patients compared with non-ulcer subjects among NSAID users. Telomere shortening is closely associated with severity of H. pylori-induced gastritis and CDH1 methylation status. Also, telomere shortening is accelerated by NSAID usage especially in H. pylori-negative subjects.

本文言語English
ページ(範囲)65-71
ページ数7
ジャーナルClinical and Experimental Medicine
16
1
DOI
出版ステータスPublished - 01-02-2016

All Science Journal Classification (ASJC) codes

  • 生化学、遺伝学、分子生物学(全般)

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