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. 2018 Aug 13;128(9):4008–4024. doi: 10.1172/JCI99287

Figure 2. Constitutive deletion of PGK-Neo from SP-CI73T-Neo mice disrupts lung development.

Figure 2

(A) Backcross of SP-CI73T-Neo founder mice to FLP-e recombinase mice generated multiple genotypes of CFlp-SP-CI73T mice, including unexcised (SP-CI73T-Neo), excised (SP-CI73T), or WT alleles. Representative ×1.5 photomicrographs of H&E-stained lungs harvested from E18.5 CFlp-SP-CI73T mice with 1 (SP-CI73T/WT) or 2 (SP-CI73T/I73T) excised SftpcI73T allele(s) reveal a graded arrest of saccular lung development. (B) Immunoblotting of E18.5 WT or Neo-excised CFlp-SP-CI73T lung homogenates for proSP-C with β-actin as a loading control. Densitometric quantitation of aberrant proSP-CI73T (arrows, bracket) and WT proSP-C (arrowheads). *P < 0.05 versus WT/WT by 1-way ANOVA with Tukey’s post hoc test. (C) Staining of E18.5 CFlp-SP-CI73T/I73T embryos for HA revealed tufts of HA+ AT2 cells within obliterated saccules. CFlp-SP-CWT/WT controls showed normal developing saccules lined by proSP-C+ cells. Scale bars: 70 μm. (D) TEM of E18.5 CFlp-SP-CI73T/I73T and CFlp-SP-CWT/WT lungs. SP-CWT/WT saccules contained intraluminal surfactant (inset). CFlp-SP-CI73T/I73T lungs contained disrupted saccules filled with poorly differentiated epithelial cells (inset). Scale bars: 10 μm. (E) Representative ×60 immunofluorescence micrographs of E18.5 lungs from CFlp-SP-CI73T/I73T, CFlp-SP-CI73T/WT, and CFlp-SP-CWT mice stained for proSP-C (green) and AQP5 (red), showing loss of AQP5 and increase in proSP-C staining in CFlp-SP-CI73T animals.