Skip to main content
. 2018 Feb 1;314(5):L860–L870. doi: 10.1152/ajplung.00365.2017

Fig. 5.

Fig. 5.

Akap1 genetic deletion promotes mitochondrial mitophagy associated markers after hyperoxia. Wild-type (wt) and Akap1−/− mice were exposed to room air or hyperoxia for 48 h, then lung protein was collected and subjected to SDS-PAGE followed by Western blotting. A: representative Western blot and densitometric analysis of PINK1 and Parkin. Data are shown as means ± SE (*P < 0.05 vs. wt room air; #P < 0.05 vs. wt hyperoxia; n = 5 mice/group). B: representative Western blot and densitometric analysis of p62. Data are shown as means ± SE (*P < 0.05 vs. wt room air; #P < 0.05 vs. wt hyperoxia; n = 5 mice/group). C: representative Western blot and densitometric analysis of LC3BII/I ratio to β-actin. Data are shown as means ± SE (**P < 0.01 vs. room air; *P < 0.01 vs. room air; **P < 0.05 vs. room air; ns, no significance; n = 5 mice/group).