Fig. 7
From: Attenuated PINK1 autophosphorylation play neuroprotective and anti-seizure roles in neonatal hypoxia
Inhibition of OMA1 expression aggravated mitophagy, mitochondrial oxidative stress, apoptosis, and neuronal damage. (A-C) Inhibition of OMA1 expression significantly increased the fluorescence intensity of LC3B (red) and TOMM20 (green) in the EC and DG (3 day; n = 4/group). DAPI, blue. Bar = 30 μm. (D-H) The changed levels of P62, active caspase-3 and caspase-3 in the cortex and hippocampus were detected by western blotting (n = 4/group). (I-L) Mito-SOX levels in the cortex and hippocampus detected by fluorescence microplate reader and flow cytometry (n = 4/group). (M,N) Neuronal damage in the DG, CA3 and EC (3 day; n = 4/group). Bar = 60 μm. Mean ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001, compared with controls (one-way ANOVA); and #P < 0.05, ###P < 0.001, compared with each other (one-way ANOVA with Dunnett’s T3 post-hoc test). C cortex, CA3 cornu ammonis area 3, DG dentate gyrus, EC entorhinal cortex, LC3B microtubule-associated protein light chain 3B, H hippocampus, Hy Hypoxia, OMA1 overlapping with the m-AAA protease 1 homolog, TOMM20 translocase of outer mitochondrial membrane 20.
