Proteomic differences with and without ozoneexposure in a smoking-induced emphysema lung model

• Published in: The Korean journal of internal medicine pp. 62 - 72
• Main Authors: 어수택, 구소미, 장안수, 박성우, 최재성, 김용훈, 박춘식
• Format: Journal Article
• Language: English
• Published: 대한내과학회 01.01.2015
• Subjects: 내과학
• ISSN: 1226-3303; 2005-6648
• DOI: 10.3904/kjim.2015.30.1.62

Background/Aims: Acute exacerbations in chronic obstructive pulmonary diseasemay be related to air pollution, of which ozone is an important constituent. In this study, we investigated the protein profiles associated with ozone-inducedexacerbations in a smoking-induced emphysema model. Methods: Mice were divided into the following groups: group I, no smoking andno ozone (NS + NO); group II, no smoking and ozone (NS + O); group III, smokingand no ozone (S + NO); and group IV, smoking and ozone (S + O). Bronchoalveolarlavage, the mean linear intercept (MLI) on hematoxylin and eosin staining, nano-liquid chromatography-tandem mass spectrometry (LC-MS/MS), and Westernblotting analyses were performed. Results: The MLIs of groups III (S + NO) and IV (S + O) (45 ± 2 and 44 ± 3 μm, respectively)were significantly higher than those of groups I (NS + NO) and II (NS+ O) (26 ± 2 and 23 ± 2 μm, respectively; p < 0.05). Fourteen spots that showed significantlydifferent intensities on image analyses of two-dimensional (2D) proteinelectrophoresis in group I (NS + NO) were identified by LC-MS/MS. The levels ofsix proteins were higher in group IV (S + O). The levels of vimentin, lactate dehydrogenaseA, and triose phosphate isomerase were decreased by both smokingand ozone treatment in Western blotting and proteomic analyses. In contrast,TBC1 domain family 5 (TBC1D5) and lamin A were increased by both smokingand ozone treatment. Conclusions: TBC1D5 could be a biomarker of ozone-induced lung injury in emphysema. KCI Citation Count: 3