p66Shc Mediates Mitochondrial Dysfunction Dependent on PKC Activation in Airway Epithelial Cells Induced by Cigarette Smoke

Figure 1

CSE increased p66Shc expression in a concentration-dependent manner in Beas-2b cells. When airway epithelial cells were exposed to CSE for 24 h, cell viability was gradually decreased at the indicated concentration (a). After 24 h stimulation with CSE (2.5–10%), real-time PCR showed that p66Shc mRNA expression was increased in a concentration-dependent manner (b). Western blot showed that the expression levels of p66Shc and p-p66Shc in the whole cell lysates were significantly increased in a concentration-dependent manner when the cells were stimulated with CSE (2.5–10%) for 24 h (c). The mitochondria were isolated from airway epithelial cells by differential centrifugation, and mitochondrial purity was confirmed by Western blot (d). p66Shc expression in the mitochondrial lysates was also significantly increased when the cells were stimulated with CSE (2.5–10%) for 24 h (e). All statistical data were obtained from three independent experiments and presented as the mean ± SD. versus the control group.

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