Fig. 2: In vivo E-cadherin knockdown in the alveolar type, I (AT1) and alveolar type II (AT2) cells have differential effects on mouse lung function and histology.
From: Loss of E-cadherin is causal to pathologic changes in chronic lung disease
To knock down E-cadherin in the AT1 cells of mice lungs, Cdh1fl/fl-AgerCre mice were fed a tamoxifen diet (TAM) for 1 month. These were compared to Cdh1fl/fl-AgerCre mice receiving a normal chow diet (ND) and Cdh1fl/fl-AgerWT receiving TAM control mice. a Total lung capacity, b compliance, and c residual volume were decreased in E-cadherin knockdown in AT1 cells of mice lung. No difference in lung histology was observed by d H & E staining (representative image at 5X with a scale bar of 500 µm) and e quantified mean linear intercepts (Lm) after E-cadherin knockdown in AT1 cells. To knock down E-cadherin in the AT2 cells of mice lungs, Cdh1fl/fl-SpcCre mice were fed TAM for 1 month. These were compared to Cdh1fl/fl-SpcCre, mice receiving ND. f Total lung capacity was increased, g compliance was increased, and h without significant changes in residual volume in E-cadherin knockdown in AT2 cells of mice lungs. Lung histology shows airspace enlargement as observed by i H & E staining (representative image at 5× with a scale bar of 500 µm) and j an increase in Lm after E-cadherin knockdown in AT2 cells. Data is expressed as median bars and generated from 5 to 15 mice per group. Kruskal-Walli’s test followed by Dunn’s multiple comparison test was performed to assess total lung capacity, compliance, and residual volume in E-cadherin knockdown in AT1 cells. Mann-Whitney test was performed to assess Lm of AT1 and AT2, and lung function tests (total lung capacity, compliance, and residual volume) in E-cadherin knockdown in AT2 cells. Data is generated from 5 to 14 mice per group. P < 0.05 were considered statistically significant.
