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Fig. 1 | Particle and Fibre Toxicology

Fig. 1

From: Attenuation of PM2.5-induced alveolar epithelial cells and lung injury through regulation of mitochondrial fission and fusion

Fig. 1

Effect of PM2.5, the DRP-1 inhibitor Mdivi-1, the OPA1 activator BGP-15 and of DRP1 knockdown (KD) and OPA1 overexpression (OE) on cell proliferation, intracellular and mitochondrial ROS in A549 cells. Cell proliferation was measured using EdU assays (A) and intracellular oxidative stress measured by DCFH (B) in A549 cells. Effect the DRP-1 inhibitor Mdivi-1 and the OPA-1 activator BGP-15 alone or in the presence of PM2.5 on cell proliferation (C) and on intracellular redox-responses (D). Effect of DRP1-KD and OPA1-OE on baseline and PM2.5–modulated cell proliferation (E) and on intracellular redox-responses (F) in A549 cells. Effect of PM2.5 in the presence and absence of Mdivi-1 and BGP-15 on mitochondrial superoxide (G) and of DRP1-KD and OPA1-OE on PM2.5-evoked mitochondrial superoxide (H) in A549 cells. The knockdown of DRP1 (I) and overexpression of OPA1 (J) in A549 cells was confirmed by Western blot. Mean values and data from individual experiments are shown. One-way ANOVA with Bonferroni’s post hoc test (for equal variance) or Dunnett’s T3 post hoc test (for unequal variance) was performed for comparisons among multiple groups. *P < 0.05, **P < 0.01, ***P < 0.001. NC = negative control shRNA, DRP1-KD = DRP1 knockdown, OPA1-OE = OPA1 overexpression

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