Conditional ablation of JNK1 from lung epithelial cells attenuates lung fibrosis induced by adTGFβ1.
JNK1 was selectively ablated from the bronchiolar epithelial cells and type II cells using a CCSP promoter driving a reverse tetracycline activator (rtTA), the tetracyclin operon driving CRE recombinase (TetOP-Cre), and mice carrying a LoxP-flanked Jnk1 allele. Assessment of total collagen content in lung tissue 3 weeks following administration of bleomycin via hydroxyproline content (A), Masson’s trichrome staining (B), Sircol assay (C) and semi-quantitative evaluation of Masson’s trichrome reactive material (D). E: Assessment of pulmonary fibrosis, using the sircol assay in response to AdTGFβ1 in mice containing the CCSP-rtTA, TetO-Cre, and Jnk1 loxP/loxP alleles, or CCSP-rtTA, TetO-Cre alleles, in the absence of doxycycline-containing food. (WT- Jnk1: AdCtr n = 6, adTGFβ1 n = 8, ΔEpi Jnk1: AdCtr n = 5, adTGFβ1 n = 8 respectively mice/group from 2 independent experiments). * p< 0.05 compared to the adCtr control groups. † p< 0.05 compared to respective WT groups. (ANOVA). Scale bars: 50 μm.