Research Paper Volume 15, Issue 24 pp 15382—15401

Proteomic analysis reveals the aging-related pathways contribute to pulmonary fibrogenesis

class="figure-viewer-img"

Figure 1. Impact of aging on mouse lung. (A) H&E and Masson staining showed that the alveolar structure of the lung tissue of 2-month-old mice was clear and intact, whereas the lung tissue of 16-month-old mice had more collagen deposition, damaged alveolar structure, and thickened alveolar walls. (B) MicroCT imaging for small animal demonstrated that some old mice had fibrous strip shadows and thickened interlobular septa compared with young mice. (C) FVC results showed that pulmonary function decreased in aging mice. (D) Western blot showed that collagen III, collagen I, vimentin, α-SMA, FAP1, S100A4, SMP30, and P16 increased significantly in aging mice, but E-cadherin and SPC decreased. (E) Immunofluorescence staining showed that α-SMA expression in lung tissues of aging mice was higher than in those of young mice. (F) Immunofluorescence images showed that SPC expression was significantly lower in lung tissue of 16-month-old mice than in that of 2-month-old mice. (G) Double immunofluorescence staining showed that P16 increased in aging mice and decreased in young mice. E-cadherin decreased in aging mice and increased in young mice. (H) Double immunofluorescence staining showed that the expression of S100A4 and P16 in the lung tissue of aging mice were significantly higher than in that of young mice.