Fig. 7.

MFN1 and MFN2 regulates surfactant lipid synthesis in AEC2 cells. a, b Representative TEM images of lamellar bodies (LB) in control, Mfn1- and Mfn2-deficient AEC2 cells at baseline (×25,000; n = 3 mice per group) and 8 days after bleomycin treatment (×50,000; n = 2 mice per group) (scale bar 500 nm) (a) and in Sftpc^CreERT2+/− and Mfn1/2^−/− AEC2 cells (×25,000; n = 3 mice per group; scale bar 1 μm) (b, left panel). Quantification of the percentage of LB with disorganized lipid membranes in AEC2 cells by TEM image analysis (×12,000) (b, right panel). Each dot represents one AEC2 cell (Sftpc^CreERT2+/− AEC2 cells n = 15 from 3 mice, Mfn1/2^−/− AEC2 cells n = 17 from 2 mice; ***p < 0.001, vs. control by unpaired Student’s t test). c, d Heat map (c) and bar graph (d) of differential changes of specific lipid contents in control, Mfn1^−/− and Mfn2^−/− AEC2 cells (n = 4 biologically independent samples per group) 8 days after bleomycin treatment. The fold-changes of specific lipids in AEC2 cells after bleomycin treatment relative to those after PBS treatment (n = 3 biologically independent samples per group) were calculated and log-transformed (base 2) (d, *p < 0.05, **p < 0.01, calculated fold change vs. 1 by unpaired Student’s t test). e Lipidomic analysis in Sftpc^CreERT2+/+ and Mfn1/2^−/− AEC2 cells (n = 4 mice per group; *p < 0.05, **p < 0.01, ***p < 0.001, vs. Sftpc^CreERT2+/+ AEC2 cells by unpaired Student’s t test). Data are presented as mean±s.e.m. (d, e). Source data (b–e) are provided as a Source Data file