Fig. 3
Loss of CXCL10 attenuates fibrotic lung remodeling of neonatal mice after hyperoxia. A-C Representative lung tissue images showing the spatial distribution of elastic fibers in mouse lungs after exposure to normoxia (21% O2, NOX) or hyperoxia (85% O2, HYX) from birth until postnatal day 14 (P14) (A). Quantitative histomorphometric analysis of septal thickness (B). Quantitative elastic fiber content relative to lung tissue (elastic fiber fraction) (C). D, E Representative images of Picro-Sirius red-stained lung sections showing collagen deposition in mouse lungs after exposure to NOX or HYX from birth until P14 (D). Quantitative analysis of the collagen amount relative to lung tissue in percentage (%, collagen fraction; E). F, G Gelatin zymography to detect matrix metalloproteinase 2 (MMP2; F) and MMP9 (G) activity along with densitometric analysis in lungs at P14 after exposure to NOX or HYX. H, I Immunoblots and respective quantification of phospho-SMAD2 protein (pSMAD2) total SMAD2 protein (downstream effector of TGFβ signaling) in lungs at P14 after exposure to NOX or HYX; β-actin was used as loading control (H). Densitometric data summary of pSMAD2 relative to total SMAD2 (I). Mean ± SEM; n = 4–9/group. Unpaired t test: $p < 0.05; Two-way ANOVA: *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; scale bar: 100X