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. 2020 Sep 20;17:276. doi: 10.1186/s12974-020-01912-3

Fig. 4.

Fig. 4

Overexpression of mortalin reduces the HIV-1 Tat mediated mitochondrial dysfunction and fragmentation. a) Percentage change in mitochondrial membrane potential (mean fluorscence intensity of JC-1 aggregates/JC-1 monomers) in indicated transfected groups after 24 h, as analyzed by fluorescence estimation (n = 5). b, c) Percentage change and representative western blot showing change in COXIV expression in all transfected PDA groups. GAPDH was used as the loading control (n = 5). d) Representative images of mitchondria labelled with mitotrackerRED after 24 h of transfection with indicated plasmids (n = 4). e) Quantitative analysis of mitochondrial length stained with mitotrackerRED (n=4). f) Representative electron microscopic images showing mitochondrial morphology in transfected groups. Arrows indicate regions showing differently shaped mitochondria (n=3). g) Quantitative analysis of mitochondrial diameter of electron microscopic images in transfected cell (n = 3). All data represent mean ± standard deviation, from independent experiments (n stands for number of independent experiments, *p< 0.05, **p< 0.005 with respect to control, #p< 0.05, ##p< 0.005 with respect to HIV-1 Tat and cotransfected group (PC stands for plasmid control and PC+PC is used as plasmid control in cotransfected cells)