Phospho-JNK immunoreactivity is increased in lung tissues in settings of airways and parenchymal fibrosis.
(A) p-JNK in lung tissue derived from mice with bleomycin or adTGFβ1-induced pulmonary fibrosis. Mice were exposed to agents, and respective vehicle controls (con), and 3 weeks thereafter, lung tissues were homogenized for the assessment of pJNK via Western blot analysis. PBS or control-adenoviral vector exposed mice resulted in similar lack of p-JNK immunoreactivity (see Fig 1B below), and therefore only one representative control group (Con) is shown. (B) Immunolocalization of p-JNK (red) in lung tissue from mice 3 weeks after exposure to a representative vehicle control, bleomycin or adenovirus expressing recombinant active transforming growth factor beta-1 (adTGFβ1). Lower Panels; Co-localization of p-JNK with CCSP in control vehicle, bleomycin or adTGFβ1. Results were evaluated via confocal microscopy. Co-localization of p-JNK and CCSP is indicated by a yellow color. Scale bars: 50 μm. (C) p-JNK (blue) in lung tissue from patients with idiopathic pulmonary fibrosis (IPF) or non-IPF lung (Normal, n = 5 patients/group). Scale bars: 300 μm.