Fig. 1
SiO2-induced pulmonary inflammation induced anoikis resistance only in HPF-a cells. A The CCK-8 assay suggested that a 6-h CM treatment significantly increased the viability of HPF-a cells (n = 5); *P < 0.05 compared with the control group. CM from macrophages treated with SiO2 increased the viability of HPF-a cells (B), BEAS-2B cells (C) and HPMECs (D) (n = 5); *P < 0.05 compared with the control group. Representative western blot and densitometry analyses of five separate experiments showing the effects of CM on the expression of the anoikis resistance marker NTRK2 in HPF-a (E), BEAS-2B (F) and HPMECs (G); (n = 5); *P < 0.05 compared with the 0-h group, **P < 0.01 compared with the 0-h group, and ***P < 0.001 compared with the 0-h group. H Sirius Red staining and Masson’s trichrome staining showed that SiO2 induced more collagen deposition and incomplete pulmonary alveoli in the lung tissues, indicating that the mouse silicosis model was successfully established. Scale bar = 100 μm. I Immunofluorescence staining shows the expression of the fibroblast marker Vimentin and the anoikis protein NTRK2 in mouse lung tissue. Scale bar = 100 μm. (J) Spatial transcriptomics showing the coexpression of Ntrk2 and Vimentin