PURPOSE: The goal of this study is to find out the differences of protein profiles between smoking-induced emphysema lung model and acute exposure of ozone on smoking-induced emphysema model.
METHODS: Mice were divided into four groups as follows; Group A, no smoking and no ozone, Group B, smoking and no ozone, Group C, no smoking and ozone, Group D, smoking and ozone. Smoking groups were exposed to five cigarettes a day for five days/week for 6 months and ozone groups were exposed to 30 PPM for 30 min after completion of smoking exposure. Bronchoalveolar lavage, mean linear intercept (MLI) on H-E stain, and protein identification by nano LC-MS/MS were performed.
RESULTS: The number of total cell counts and percentage of neutrohil count in BAL fluid significantly increased in Group C and D compared to those in group A and B (p<0.05). The mean linear intercept (μm) of group C and group D (34±3, 32±2, respectively) significantly more increased than those in group A and B (24±3, 25±2, respectively) p<0.05). Thirteen spots, which showed significantly different intensities on image analyses of 2D-protien electrophoresis, were identified by LC-MS/MS. Unfortunately, we could not find the protein which increased only in group D. Increased proteins in group C and D were transgelin-2, apolipoprotien A, glutathione S transferase, and Xin-beta. Decreased proteins in group C and D were ribonucleoprotein, copine-1, cytochrome b1, annexin A2, histone H4, and novel protein.
CONCLUSIONS: Several proteins could be biomarkers of ozone-induced lung injury on emphysema.
CLINICAL IMPLICATIONS: This model can be a model of acute exacerbation of COPD (chronic obstructive pulmonary disease) and further studies can find biomarkers of acute exacerbation of COPD.
DISCLOSURE: The following authors have nothing to disclose: Soo-taek Uh, Yang Ki Kim, Ki Up Kim, Sung Woo Park, An Soo Jang, Dojin Kim, Choon Sik Park
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