SU, BH, Tseng, YL, Shieh, GS, Chen, YC, Shiang, YC, Wu, P, Li, KJ, Shiau, AL and Wu, CL (2013) Prothymosin α overexpression contributes to the development of pulmonary emphysema. Nature Communications, 4 (1).

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Abstract

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.

Item Type: Article
Additional Information: This article has been published with Gold Open Access by Nature Communications
Uncontrolled Keywords: biological sciences; cell biology; medical research
Subjects: Q Science > QH Natural history > QH301 Biology
R Medicine > R Medicine (General)
Divisions: Faculty of Medicine and Health Sciences > Institute for Science and Technology in Medicine
Depositing User: Symplectic
Date Deposited: 21 Mar 2016 11:06
Last Modified: 24 May 2019 15:06
URI: http://eprints.keele.ac.uk/id/eprint/1588

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