Fig. 2: Lung-specific overexpression of FOXN3 impedes the progression of pulmonary fibrosis.
From: Phosphorylation of FOXN3 by NEK6 promotes pulmonary fibrosis through Smad signaling
a Quantitative PCR analysis showing the RNA expression levels of WT and Foxn3LSL KI mice following BLM induction (n = 4). b Western blot analysis showing FOXN3 protein levels in the lungs of WT and Foxn3LSL KI mice (n = 4). c Histological trichrome staining analysis comparing the fibrotic response in the lungs of WT and Foxn3LSL KI mice following BLM induction. Scale bars, 100 μm. d H&E staining analysis showing the inflammatory response in the lungs of WT and Foxn3LSL KI mice following BLM induction. Scale bars, 100 μm. e Enzyme-linked immunosorbent assays (ELISA) showing the levels of TNFα in the BAL fluid from the WT and Foxn3LSL KI mice upon BLM induction (n = 5). f ELISA analysis showing the levels of IL-6 in the BAL fluid from the WT and Foxn3LSL KI mice upon BLM induction (n = 5). g Quantitative PCR analysis showing the RNA levels of the pro-fibrotic factors in the lungs of WT and Foxn3LSL KI mice following BLM induction (n = 4). h Quantitative PCR analysis showing the RNA levels of the pro-fibrotic factors in primary pulmonary fibroblasts isolated from WT and Foxn3LSL KI mice following BLM stimulation (n = 3). i Hydroxyproline measurements comparing the collagen content in the lungs of WT and Foxn3LSL KI mice, with or without BLM stimulation (n = 4). The data (e and f) were assessed by two-tailed Student’s t test and the data (a) and (g–i) were assessed by one-way ANOVA. All data are shown as the mean ± SD.
