Fig. 2

Efferocytosis function is impaired while MERTK is elevated in lung macrophages from mice with bleomycin-induced pulmonary fibrosis. A Efferocytosis of mouse lung macrophages under fluorescence microscope. As indicated by white arrowheads, macrophages (F4/80 + , red) recognize and phagocytize apoptotic bodies of MLE12 (CFSE + , green). B Flow cytometry analysis of mouse lung macrophage efferocytosis. Lung macrophages were pre-gated on F4/80 + area, ratio and capacity of macrophage efferocytosis were measured by CFSE-positive ratio (CFSE + /[CFSE + F4/80 +]) and MFI of CFSE, respectively (NS, n = 11; BLM, n = 9; BLANK: macrophages were cultured without addition of apoptotic cells). C Flow cytometry analysis of mitochondrial membrane potential of mouse lung macrophages. Lung macrophages were pre-gated on F4/80 + area, and the mean fluorescence intensities of JC-1 monomers (FITC) and aggregates (PE) were analyzed by flow cytometry (NS, n = 17; BLM, n = 14). D After staining with JC-1, the fluorescence staining of lung macrophages was observed under a fluorescence microscope. Mitochondrial membrane potential was semi-quantified by the ratio of the mean fluorescence intensity of JC-1 aggregates (red) to JC-1 monomers (green) (NS, n = 8; BLM, n = 7). E The mRNA expression of MERTK, CD36 and Rac1 in mouse lung macrophages was detected by qRT-PCR (n = 7–12 mice per group). Data were presented as mean ± SEM. T-tests or Mann–Whitney tests were used for two-group (NS and BLM) comparsions. *p < 0.05; **p < 0.01; ***p < 0.001; n.s., not significant