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. 2023 Jul 24;8(14):e167211. doi: 10.1172/jci.insight.167211

Figure 4. AT2 proliferation is NF-κB dependent in LPS-treated β1AT2-KO lungs.

Figure 4

(A) Representative images of BrdU-incorporated precision-cut lung slices (PCLS) treated with LPS and/or NF-κB inhibitor BAY 11-7082 for 48 hours. Slices were immunostained for BrdU (cyan) and pro–SP-C (magenta) with DAPI nuclear marker (white). (B) Quantification of proliferating AT2 cells by percentage of total AT2 cells (BrdU+pro–SP-C+ over total number of SP-C+ cells) by condition as indicated (n = 6–8 mice/group, 1 slice per mouse per condition, imaged and quantified 10 original magnification, 40× sections/mouse per condition, data from 5 separate experiments; P = 0.0010, F value = 6.3 for treatment variation; P < 0.0001, F value = 26.1 for genotype variation). Two-way ANOVA was used to compare treatment conditions and genotype in B. * P < 0.05. Scale bar = 100 μm for low-power images in A, 50 μm for inset in A.