Prothymosin α overexpression contributes to the development of pulmonary emphysema

Bing-Hua Su, Yau-Lin Tseng, Gia-Shing Shieh, Yi-Cheng Chen, Ya-Chieh Shiang, Pensee Wu, Kuo-Jung Li, Te-Hsin Yen, Ai-Li Shiau, Chao-Liang Wu

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25 Citations (Scopus)


Emphysema is one of the disease conditions that comprise chronic obstructive pulmonary disease. Prothymosin α transgenic mice exhibit an emphysema phenotype, but the pathophysiological role of prothymosin α in emphysema remains unclear. Here we show that prothymosin α contributes to the pathogenesis of emphysema by increasing acetylation of histones and nuclear factor-kappaB, particularly upon cigarette smoke exposure. We find a positive correlation between prothymosin α levels and the severity of emphysema in prothymosin α transgenic mice and emphysema patients. Prothymosin α overexpression increases susceptibility to cigarette smoke-induced emphysema, and cigarette smoke exposure further enhances prothymosin α expression. We show that prothymosin α inhibits the association of histone deacetylases with histones and nuclear factor-kappaB, and that prothymosin α overexpression increases expression of nuclear factor-kappaB-dependent matrix metalloproteinase 2 and matrix metalloproteinase 9, which are found in the lungs of patients with chronic obstructive pulmonary disease. These results demonstrate the clinical relevance of prothymosin α in regulating acetylation events during the pathogenesis of emphysema.
Original languageChinese (Traditional)
JournalNature Communications
Issue number1
Publication statusPublished - 2013
Externally publishedYes

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