Figure 4. Increased EMAPII in human COPD.

(A) Secreted EMAPII in the acellular BALF from otherwise healthy active smokers (triangles; n = 9) compared with that from nonsmokers (circles; n = 10). Mean arbitrary units measured by densitometry were normalized by protein concentration (AU/μg/ml; mean ± SD, *P = < 0.01, t test). (B) Box plot of secreted mature EMAPII in acellular BALF from healthy nonsmokers, ex-smokers without COPD, or ex-smokers with COPD shown in arbitrary units normalized by vinculin densitometry units (*P < 0.05, ANOVA; n = 15/group). Demographic and clinical data are shown in Supplemental Table 1. (C) EMAPII detection by immunostaining with polyclonal EMAPII antibody (red, arrows; DAPI-nuclei are stained in blue) in lung parenchyma of patients with emphysema (bottom panels) compared with subjects without lung disease (normal lung, top panel). Note intense EMAPII staining in the alveolar wall (alv; inset) in emphysematous lungs. IF, immunofluorescence. Scale bar: 50 μm. (D) Box plot of lung EMAPII expression in lung sections from subjects without lung disease (normal; n = 4), with emphysema (emphys; n = 9), or with usual interstitial pneumonitis (UIP; n = 13) (immunohistochemistry staining arbitrary units; *P < 0.05 versus normal, ANOVA). (B and D) Lines within the boxes show medians; bounds of the boxes show 25th and the 75th percentiles of the data, respectively; and whiskers show outliers (5th and 95th percentiles, respectively).