Fig 1: Effects of LCMR1 deletion on the AT2 cell number and pulmonary surfactant proteins. (A) Representative images of immunofluorescence staining for proSP-C (red) in lung sections from LCMR1flox/flox and LCMR1?AT2 mice on day 14 after tamoxifen administration. The nuclei were stained with DAPI (blue). Scale bars, 50 µm. (B-E) qPCR analysis of the mRNA expressions of SP-A (B), SP-B (C), SP-C (D), and SP-D (E) in the lung tissue from LCMR1flox/flox and LCMR1?AT2 mice on day 14 after tamoxifen administration, normalized to ß-actin (n=4/group). (F,G) Western blot (F) and quantitative analysis (G) of the protein expressions of SP-A, SP-B, SP-C, and SP-D in lung tissues from LCMR1flox/flox and LCMR1?AT2 mice on day 14 after tamoxifen administration, normalized to a-tubulin (n=3/group). Data are presented as the mean ± SEM. *, P<0.05, **, P<0.01, ***, P<0.001; NS, not significant by unpaired Student’s t-test. AT2, alveolar type II; LCMR1, lung cancer metastasis-related protein 1; SEM, standard error of mean.