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. Author manuscript; available in PMC: 2009 May 6.
Published in final edited form as: Neurotox Res. 2008 Dec;14(4):367–382. doi: 10.1007/BF03033861

FIGURE 2. Unregulated mitochondrial GSK3β activity facilitates apoptosis induced by mitochondrial complex I inhibition, but not complex II inhibition, ER stress, nor genotoxic stress.

FIGURE 2

A. mS9AGSK3β or mGFP cells were treated with Dox (1 µg/ml) for 24 h in serum-containing media and were transferred to serum free media containing Dox for 1 h prior to treatment with 5 mM 1-methyl-4-phenylpyridinium (MPP+), 5 µM rotenone (ROT), 2 µM thapsigargin (TG), 1 µM camptothecin (CT), or 20 mM 3-nitropropionic acid (3-NP) for 4 h, and total cell lysates were immunoblotted for PARP. Quantitation of the proteolyzed PARP band for each sample is based on the percent of proteolyzed PARP from each sample's matched Dox- cells treated with the different apoptosis inducers. Values are means ± S.E.M., n=3, *P <0.05, ANOVA. B. Non-induced and induced mGFP cells were treated with 5 µM rotenone or 5 mM MPP+ for 4 h, and total cell lysates were immunoblotted for PARP. mS9AGSK3β cells were treated with Dox (1 µg/ml) for 24 h in serum-containing media and were transferred to serum free media containing Dox for 1 h and (C) 5 µM 2-thio(3-iodobenzyl)-5-(pyridyl)-[1,3,4]-oxadiazole (inhib II) or (D) 20 mM lithium for 30 min prior to treatment with 5 mM MPP+ or 5 µM rotenone for 4 h. PARP proteolysis was measured by Western blot analysis.