Figure 3
From: Hyperoxia prevents the dynamic neonatal increases in lung mesenchymal cell diversity
Developmental changes in perinatal fibroblasts, myofibroblasts, and airway smooth muscle. (A) Changes in composition of lung fibroblast subtypes between E18.5 and P21. (B) Embedding of fibroblasts and precursors at E18.5 (left) and P1 (right). (C) Distribution of expression for Col13a1 and Col14a1 in fibroblasts. (D) Pathways enriched among genes up- (red, top) or down-regulated (blue, bottom) in early postnatal fibroblasts versus prenatal fibroblast precursors38. (E) Changes in abundance of ASM, myofibroblasts and their precursors between E18.5 and P1. (F) Embedding of ASM and myofibroblasts at E18.5 (left) and P1 (right). (G) Distribution of expression of Hhip and Pdgfra in myofibroblasts, and early ASM, and their precursors. (H) Pathways enriched among genes up- (red, top) or down-regulated (blue, bottom) in early postnatal myofibroblasts and ASM versus their precursors. (I) Expression changes of Crh between E18.5 and P1. (J) In-situ hybridization of Crh+ Tgfbi+ (solid arrows) and Crh- Tgfbi+ cells (dashed arrows) in E18.5 and P1 lungs. (K) Expression changes of Hsd11b1 in fibroblasts and Hif3a in both fibroblasts, ASM, and myofibroblasts between E18.5 and P1. (L) Fraction of proliferative fibroblasts and myofibroblasts at postnatal time points. (M) In-situ hybridization of nonproliferating (Mki67− solid arrows) and proliferating (Mki67+ dashed arrows) myofibroblasts at P7. (N) Embedding of Early ASM and myofibroblasts, colored by subtype and by expression of select genes. (O) In-situ hybridization of P7 lungs around airways (left) and in the distal lung (right). Dashed arrows: Tgfbi+ Hhip+ cells, solid arrow: Tgfbi+ Pdgfra+ cells. (P) Quantification of the degree of coexpression of Hhip, Tgfbi, and Pdgfra from in-situ images of P7 mice. P-values are Kolmogorov–Smirnov tests with Bonferroni multiple hypothesis correction.
