Cumulative effects of dopamine and mutated huntingtin on mCII expression and catalytic activity

Abstract

Measurement of Ip and Fp protein expression levels as indicated by western blotting, and mCII activity in striatal cultures treated for 24 h with increasing concentrations of DA. () Representative western blot showing the reduction of Ip and Fp expression, while levels of the alpha-subunit of complex V (C-V) remain essentially unchanged. () Quantification of protein levels for Ip and Fp after western blotting. () Dose-dependent effect of a 24 h DA treatment on the catalytic activity (succinate dehydrogenase) of mCII. () Quantification of protein levels for Bcl, the alpha-subunit of complex V (C-V), subunit 4 of complex IV (C-IV) and the 39 kDa subunit of complex I (C-I) after 100 µ DA treatment. () Changes in Ip and Fp mRNA levels over time during a 100 µ DA treatment, using quantitative RT–PCR. Note the transient down-regulation of both transcripts. () mCII activity in striatal neurons transduced with lentiviral Htt171-82Q (mutant) or Htt171-19Q (wild-type), before treatment with 100 µ DA or vehicle. The effects of DA and mutated Htt on the reduction of mCII activity are cumulative, and correspond to the synergistic effects on neuronal degeneration seen in Figure . * < 0.05; ** < 0.001; < 0.01; ANOVA and Fisher's PLSD test.<p><b>Copyright information:</b></p><p>Taken from "Dopamine determines the vulnerability of striatal neurons to the N-terminal fragment of mutant huntingtin through the regulation of mitochondrial complex II"</p><p></p><p>Human Molecular Genetics 2008;17(10):1446-1456.</p><p>Published online 11 Feb 2008</p><p>PMCID:PMC2367694.</p><p>© 2008 The Author(s)</p