Figure 5. Overabundant AT2 cells are transcriptionally distinct during repair in β₁^AT2-KO mice.

(A) Uniform manifold approximation and projection (UMAP) of all epithelial cells from β₁^fl/fl and β₁^AT2-KO lungs with/without LPS clustered by label transfer from Strunz et al. (11). (B) Individual epithelial populations by group reveal transcriptionally distinct AT2s and activated AT2s in day 7 LPS-treated β₁^AT2-KO lungs. (C) Ingenuity Pathway Analysis (QIAGEN) on combined AT2 groups from uninjured β₁^fl/fl and β₁^AT2-KO lungs demonstrates upregulation of oxidative stress, senescence, and inflammatory pathways in β₁^AT2-KO lungs compared with β₁^fl/fl lungs. (D) Ingenuity Pathway Analysis shows upregulation of actin cytoskeleton signaling pathways in β₁^AT2-KO AT2 cells compared with β₁^fl/fl AT2 cells at 7 days after LPS treatment.