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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Exp Neurol. 2014 Sep 28;263:244–253. doi: 10.1016/j.expneurol.2014.09.016

Figure 1.

Figure 1

Overexpression of ALDH2 protects against rotenone-induced cell death. (A) SH-SY5Y cells were stably transfected with cDNA of FLAG-tagged wild-type (WT) or inactive (E504K) ALDH2*2. Stable clones were subfractionated into mitochondrial (Mit) and cytosolic (Cyto) fractions. Western blot analysis using anti-FLAG antibody indicated that ALDH2 was selectively expressed in the mitochondrial fraction of SH-SY5Y cells. Cytochrome c oxidase subunit IV (COX-IV) was used as an internal control for mitochondrial fraction. (B) Control cells and stable clones expressing WT ALDH2 or (E504K) ALDH2*2 were plated onto 96-well plates and allowed to adhere overnight. Cell Counting Kit-8 was used to analyze cell survival. Rotenone treatment (100 nM) for 24 hours caused a significant reduction of cell viability in control cells. Overexpression of WT ALDH2, but not (E504K) ALDH2*2 significantly protected against rotenone-induced cell death. Each bar represents the mean ± SD value of five independent experiments. *p< 0.05, **p<0.01, ***p<0.001 compared to rotenone-treated cells. Mit: mitochondrial; Cyto: cytosol fraction; WT: wild-type; E504K: (E504K) ALDH2 mutant.