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. 2015 May 1;10(5):e0123187. doi: 10.1371/journal.pone.0123187

Fig 2. p53-mediated induction of PAI-1 expression contributes to increased pulmonary MPO levels in mice with PCSE.

Fig 2

(A) WT mice were exposed to ambient air (control) or PCS (n = 5/group) for 20 weeks. LL collected from these mice was subjected to total cell counting. (B) Total protein in the lavage was quantified from the above exposed mice. (C) Paraffin embedded lung sections from WT, p53- and PAI-1-deficient mice (n = 5mice/group) exposed to ambient air (control) or PCS for 20 weeks were subjected to H&E staining. Representative fields from 1 of 3 sections per subject are shown at X 400 magnification. Lung sections were subjected to IHC analysis for neutrophils using anti-MPO antibody and for macrophages using anti-F4/80 antibody. Neutrophils (D) and macrophages (E) were counted in 10 high-power fields (hpf) are shown as bar graph. (F) Lung homogenate from WT, p53- and PAI-1-deficient mice exposed to ambient air or PCS for 20 weeks were immunoblotted for changes in the levels of MPO using anti-MPO antibody. These membranes were later stripped and analyzed for β-actin to assess loading. Data shown in bar graphs are mean ± SD of two independent experiments (n = 5 mice/group). Differences between treatments are statistically significant *(P<0.05).