論文

査読有り
2012年8月

Increase of 27-Hydroxycholesterol in the Airways of Patients With COPD

CHEST
  • Takashi Kikuchi
  • Hisatoshi Sugiura
  • Akira Koarai
  • Tomohiro Ichikawa
  • Yoshiaki Minakata
  • Kazuto Matsunaga
  • Masanori Nakanishi
  • Tsunahiko Hirano
  • Keiichirou Akamatsu
  • Satoru Yanagisawa
  • Kanako Furukawa
  • Hiroki Kawabata
  • Masakazu Ichinose
  • 全て表示

142
2
開始ページ
329
終了ページ
337
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1378/chest.11-2091
出版者・発行元
ELSEVIER

Background: 27-Hydroxycholesterol (27-OHC) is produced from cholesterol by sterol 27-hydroxylase as an intermediate in the biosynthesis pathway of bile acid. Recently, 27-OHC was reported to cause inflammation and apoptosis in various types of cells. The aim of this study was to assess the production of 27-OHC in the airways of patients with COPD and to elucidate the possible role of 27-OHC in the tissue fibrosis of COPD.Methods: Lung tissues were obtained from six control subjects and six patients with COPD, and sputum samples were obtained from 11 healthy subjects and 15 patients with COPD. The expression of sterol 27-hydroxylase in the lung was investigated by immunohistochemistry. The amounts of 27-OHC in the sputum were quantified by the liquid chromatography-tandem mass spectrometry method. Because peribronchial fibrosis in peripheral airways is involved in the airflow limitation of COPD, we investigated the profibrotic effects of 27-OHC in vitro.Results: The expression of sterol 27-hydroxylase was significantly enhanced in the lung tissues of patients with COPD compared with control subjects. The amounts of 27-OHC in the sputum were significantly increased in the patients with COPD (P < .01), and the degree of 27-OHC production was negatively correlated with lung function (P < .01). 27-OHC augmented the differentiation of lung fibroblasts into myofibroblasts and the production of extracellular matrix protein through activation of nuclear factor-kappa B and subsequent transforming growth factor-beta(1) upregulation.Conclusions: 27-OHC production is enhanced in the airways of patients with COPD and might be involved in the pathogenesis of COPD. CHEST 2012; 142(2):329-337

リンク情報
DOI
https://doi.org/10.1378/chest.11-2091
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/22281802
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000307418200014&DestApp=WOS_CPL
ID情報
  • DOI : 10.1378/chest.11-2091
  • ISSN : 0012-3692
  • eISSN : 1931-3543
  • PubMed ID : 22281802
  • Web of Science ID : WOS:000307418200014

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