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RAGE ‐ligands axis: A new ‘driving force’ for cigarette smoke‐induced airway inflammation in COPD ?
Author(s) -
Li Min,
Guo Lingli,
Wang Hao,
Wang Tao,
Shen Yongchun,
Liao Zenglin,
Wen Fuqiang,
Chen Lei
Publication year - 2015
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/resp.12557
Subject(s) - rage (emotion) , medicine , copd , hmgb1 , inflammation , glycation , small interfering rna , immunology , receptor , s100a9 , airway , messenger rna , cigarette smoke , rna , gene , neuroscience , biochemistry , chemistry , biology , anesthesia , environmental health
Receptor for advanced glycation end products ( RAGE ) was recently shown to contribute to cigarette smoke ( CS )‐induced airway inflammation in chronic obstructive pulmonary disease ( COPD ). In this study, RAGE small interfering ribonucleic acid (RNA) transfection attenuated increased messenger RNA levels of common RAGE ligands HMGB 1, S 100 A 8, S 100 A 9 and S 100 A 12, but not S 100 B following exposure to CS extract. Our findings and those from recent studies suggest a positive feedback involving RAGE and its ligands as a new ‘driving force’ for CS ‐induced airway inflammation in COPD .
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