A single bleomycin challenge was used to induce pulmonary fibrosis in WT and Fbln1c^–/– mice that were assessed 28 days later. Controls received PBS. (A) Fbln1c and (B) Fbln1d mRNA levels in whole lungs determined using quantitative real-time PCR (qRT-PCR) (n = 6–8). (C) Lung sections were stained with Verhoeff-Van Gieson stain (left, scale bar: 500 μm; insets show expanded images of indicated regions; scale bar: 50 μm) and areas of collagen around small airways quantified with normalization to the Pbm (right, n = 8). (D) Total collagen levels were assessed by measuring hydroxyproline (left) and soluble collagen (right) in the whole lung tissues (n = 8). (E) Type I collagen (Col1a1) mRNA levels were measured in whole lungs using qRT-PCR (n = 8). (F) Col1a1 protein levels were measured in whole lungs using immunoblot (left), and fold change was quantified with normalization to β-actin (right, n = 8). (G) Collagen fibers were detected by second harmonic generation (SHG) microscopy (left), and fiber areas were calculated by forward (F_SHG)/backward (B_SHG) SHG ratios (right, n = 4–6; scale bar: 100 μm). Lung function in terms of (H) tissue damping, (I) tissue elastance, and (J) lung compliance was measured using invasive plethysmography and the forced oscillation technique (n = 5–8). Statistical differences were determined with 1-way ANOVA followed by Bonferroni’s posttest. *P < 0.05, **P < 0.01, and ****P < 0.0001 compared with PBS-challenged WT or Fbln1c^–/– controls. ^†P < 0.05, and ^††P < 0.01 compared with bleomycin-challenged WT controls. NS, not significant.