Figure 4 | Scientific Reports

Figure 4

From: Dynamic expression of HOPX in alveolar epithelial cells reflects injury and repair during the progression of pulmonary fibrosis

Figure 4

Expression and localization of HOPX in control (donor) and IPF lungs. In silico analysis from Lung Genomics Research Consortium (LGRC) of (A) HOPX mRNA expression in organ donor (control) and IPF lungs, (B) correlation between HOPX mRNA expression and DLco (blue dots: control, red dots: IPF). (C) Correlation between HOPX mRNA and MMP7 mRNA in control (blue dots) and IPF (red dots) in silico. QRT-PCR analysis of (D) HOPX mRNA, (E) SFTPC mRNA, and (F) ACTA2 mRNA from whole lung homogenate of control and IPF lungs in our cohort. (G) Immunohistochemical staining of serial sections of control and IPF lung tissue for KRT5, proSP-C, HOPX, KRT7, and Ki67. In IPF lungs, proSP-C+/KRT7+ cells revealed cytoplasmic or in part nuclear expression of HOPX without nuclear Ki67 (Indicated by arrows in panels 1–4). ProSP-Clow/KRT7+ AECs of IPF-lungs also indicated robust HOPX-immunoreactivity with nuclear Ki67 expression (asterisks in panel 2 and 4). Some proSP-C+/KRT7+ cells without HOPX immunoreactivity were observed in the area of relatively preserved alveolar septa (white arrowheads in panel 5). KRT5+/KRT7+ bronchiolar basal cells did not express HOPX, and indicated nuclear expression of Ki67 (Indicated by black arrowheads in panel 2). (H) Immunohistochemical staining of serial sections of control donor lung tissues for KRT5, proSP-C, HOPX, KRT7, and Ki67. In donor lungs, HOPX expression was present in proSP-C+/KRT7+ ATII (arrows) and proSP-Clow/KRT7+ AECs (asterisks) (panels 2 and 3 in Fig. 4O), and faint in normal bronchiolar epithelium. ProSP-Clow/KRT7+ AECs expressing HOPX also revealed nuclear Ki67 expression (indicated by asterisks). In silico single cell RNA sequence analysis of (I) HOPX, (J) SFTPC, (K) KRT7, (L) CTNNB1, and (M) CTND1 in EpCAM+/HTII280+ cells. *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.0001.