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ID 48655
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著者
Iwamoto, Hiroshi 大学院医歯薬保健学研究科(医) 広大研究者総覧
Gao, Jing
Pulkkinen, Ville
Tuula, Toljamo
Nieminen, Pentti
Mazur, Witold
抄録(英)
Background: The receptor for advanced glycation end-products (RAGE) is highly expressed in the lung, where it is believed to have a homeostatic role. Reduced plasma levels of soluble RAGE (sRAGE) have been reported in patients with chronic obstructive pulmonary disease (COPD). The aim of the present study was to evaluate the association of plasma sRAGE levels with a longitudinal decline of lung function. We have also measured plasma levels of high mobility group box 1 (HMGB1), a RAGE ligand which has been associated with chronic inflammatory diseases including COPD.
Methods: Baseline plasma concentrations of sRAGE and HMGB1 were measured in non-smokers (n = 32), smokers without COPD (n = 212), and smokers with COPD (n = 51), and the associations of the plasma sRAGE and HMGB1 levels with longitudinal declines of lung function during a 4-year follow-up period were analysed.
Results: The plasma levels of sRAGE were significantly lower in smokers without COPD and in smokers with COPD, as compared to those of non-smokers. Plasma sRAGE levels positively correlated with FVC and FEV1 and inversely correlated with BMI and pack-years. Lower sRAGE levels were associated with greater declines of FEV1/FVC over 4 years in all participants. Moreover, multivariate regression analysis indicated that the baseline plasma sRAGE concentration was an independent predictor of FEV1/FVC decline in all groups. A subgroup analysis showed that decreased sRAGE levels are significantly associated with a more rapid decline of FEV1/FVC in smokers with COPD. There was no significant correlation between plasma HMGB1 levels and longitudinal decline of lung function.
Conclusions: Lower plasma concentrations of sRAGE were associated with greater progression of airflow limitations over time, especially in smokers with COPD, suggesting that RAGE might have a protective role in the lung.
内容記述
This work was financially supported by the EVO funding of the Helsinki University Central Hospital, Research Funds of the University of Helsinki, Finnish Anti-tuberculosis Association Foundation, and partly by the SalWe Research program for IMO (Tekes - the Finnish Funding Agency for Technology and Innovation grant 648/10). Jing Gao is further supported by the China Scholarship Council (CSC), CIMO, and HES-Foundation.
掲載誌名
BMC Pulmonary Medicine
14巻
開始ページ
68
出版年月日
2014-04-24
出版者
BioMed Central Ltd.
ISSN
1471-2466
出版者DOI
PubMedID
言語
英語
NII資源タイプ
学術雑誌論文
広大資料タイプ
学術雑誌論文
DCMIタイプ
text
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application/pdf
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権利情報
© 2014 Iwamoto et al.; licensee BioMed Central Ltd. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
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部局名
医歯薬保健学研究科