Fig. 2
From: AIF-regulated oxidative phosphorylation supports lung cancer development
Loss of AIF compromises OXPHOS and impairs mitochondrial structure in lung tumor cells. a Western blotting for AIF protein and the indicated OXPHOS complex I proteins in primary pneumocytes isolated from Aiffl/y KrasG12D and Aif+/y KrasG12D mice and consequently transfected with Ad5-CMV-Cre-eGFP in vitro. GAPDH was used as a loading control. b, c Representative OCR (b) and comparison (means ± SEM) of basal respiration, ATP production and maximal respiration (c) in primary pneumocytes isolated from Aiffl/y KrasG12D and Aif+/y KrasG12D mice and consequently transfected with Ad5-CMV-Cre in vitro. d Western blotting for AIF protein and the indicated OXPHOS complex I proteins in pneumocytes isolated from Aiffl/y KrasG12D and Aif+/y KrasG12D mice 6 weeks after Ad5-CMV-Cre inhalation. β-actin was used as a loading control. e Representative OCR analysis of purified transformed pneumocytes isolated from Aiffl/y KrasG12D and Aif+/y KrasG12D mice 6 weeks after Ad5-CMV-Cre inhalation. f Representative electron microscopy images for tumor tissues isolated from Aif+/y KrasG12D (upper panels) and Aiffl/y KrasG12D mice (lower panels) 18 weeks after Ad5-CMV-Cre inhalation. Note normal mitochondrial morphology with mostly intact cristae in AIF-competent tumors in contrast to swollen mitochondria with notable cristolysis in Aif-deficient lung tumor tissues (yellow arrows). Asterisks indicate lamellar bodies (Corpuscula lamellariae), rare cell organelles containing surfactant lipoproteins characteristic for type II pneumocytes. N indicates nuclei. Scale bars, 5 μm for left panel and 2 μm for right panel
