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. 2018 Sep 20;3(18):e99574. doi: 10.1172/jci.insight.99574

Figure 1. Identification of Lama1 as a genetic modifier of TGF-β–stimulated pulmonary fibrosis.

Figure 1

Lungs from 6- to 8-week-old WT and TGF-β1–Tg mice on the noted genetic backgrounds were evaluated after the mice were given doxycycline in drinking water for 14 days of to induce Tg. (A) Mallory trichrome evaluation (left panel) and total collagen content measured by Sircol collagen assay (right panel) of lungs from WT and TGF-β1 Tg mice on C57BL/6J (C57) and BALB/cJ (BALB/c) backgrounds. Scale bars: 25 μm. (B) Levels of collagen in lungs from WT and Tg mice on 10 different background strains were measured by Sircol evaluations (n = 7 for each). (C) Illustration of haplotype blocks of Lama1, Wisp1, and Hba-a1. The haplotype of each gene is represented by a colored block, and is presented in the same order as the phenotypic data shown in B. (D) Kinetic evaluation (using qRT-PCR) of the levels of mRNA encoding Lama1 in lungs from WT and TGF-β1 Tg mice on C57 and BALB/c backgrounds at various time points after transgene induction with doxycycline (DOX). (E) Expression of Lama1 mRNA in the lungs of bleomycin-challenged C57 and BALB/c mice. The histology shown in A is representative of at least 5 mice per each group. The values in A, B, D, and E represent mean ± SEM of a minimum number of 5 mice in each group. Post-Bleo, days after bleomycin challenge. *P < 0.05. **P < 0.01. #P < 0.001.