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. 2019 Nov 25;33(12):13617–13631. doi: 10.1096/fj.201901123R

Figure 2.

Figure 2

Mitochondrial dysfunction in APN−/− mice also relates to impaired mitophagy and NLRP3-inflammasome activation in lung endothelium. A, B) Western blot analysis for autophagy markers beclin-1, LC3B-II/I ratio, p62 proteins in whole lung tissues and in freshly isolated lung ECs in APN−/− and WT control mice at bsl. GAPDH is used as loading control. C, D) Western blot analysis for mitophagy markers Pink1 and Parkin in whole lung tissues and in cytosol and mitochondrial fractions isolated from lungs of APN−/− and WT control mice at bsl. GAPDH and voltage-dependent anion channels (DVAC) are used as loading control. E) Increased mt-ROS production (MitoSox) in isolated ECs from the lungs of APN−/− and WT control mice are shown in red and merged with nuclear stain DAPI in blue. F, G) Western blot analysis for NLRP3-inflammasome activation markers NLRP3, activated caspase-1, and cleaved IL-1β in the whole lung tissues and in freshly isolated lung ECs in APN−/− and WT control mice at bsl. GAPDH is used as loading control. Densitometry analyses are shown on the right; n = 6–8 in each group. Data are expressed as means ± se. Scale bars, 200 µm. *P < 0.05, **P < 0.01.