Fig. 4: Increased apoptosis induction and reduced proliferation in lungs of TRAIL^−/− compared to wildtype mice exposed to hyperoxia.

A Immunofluorescence staining for cleaved Caspase-3 (cl-Casp-3) positive cells of lung tissues from mice from Fig. 2A. Cleavage of Caspase-3 was detected in the lungs of newborn mice exposed to 40% and 85% of oxygen. B Quantification of cl-Casp-3 positive cells from A. Hyperoxia-induced cleavage of Caspase-3 was significantly increased in TRAIL^−/− compared to wildtype animals at 85% of oxygen. C Immunofluorescence staining for TUNEL positive cells of lung tissues from mice from Fig. 2A. Hyperoxia-induced apoptosis induction in the lungs of newborn mice was apparent at 40% and 85% of oxygen. D Quantification of TUNEL positive cells from C. Hyperoxia-mediated apoptosis induction was significantly increased in TRAIL^−/− compared to wildtype animals at 85% of oxygen. E Immunofluorescence staining for ki67 positive cells of lung tissues from mice from Fig. 2A. Hyperoxia-induced reduction of ki67 positive cells was present at 40% and 85% of oxygen. F Quantification of ki67 positive cells from E. Hyperoxia-induced reduction of ki67 positive cells was significantly increased in TRAIL^−/− compared to wildtype animals at 85% of oxygen. G Western blot analysis of p-IκBα and IκBα from lungs from mice from Fig. 2A. Wildtype and TRAIL^−/− mice displayed equivalent phosphorylation of IκBα at 21% of oxygen. p-IκBα levels increased only in wildtype mice exposed to hyperoxia. H Quantification of p-IκBα from G. Levels of p-IκBα remained unchanged in TRAIL^−/− mice while phosphorylation of IκBα significantly increased in wildtype animals at 40% and 85% of oxygen. Data are presented as mean + SEM. Statistical analysis was performed by t-test. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. n ≥ 6 mice/group.