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. Author manuscript; available in PMC: 2015 Nov 4.
Published in final edited form as: Cell Metab. 2014 Nov 4;20(5):840–855. doi: 10.1016/j.cmet.2014.10.005

Fig. 7. PARP inhibition or NAD+ replenishment rescues CS associated alterations in mice and human cells.

Fig. 7

(A) Measurements of the oxygen consumption rate using the Seahorse XF24 analyzer while adding increasing doses of the PARP inhibitors 3AB, NU1025 or PJ34 (n=3 separate experiments, mean ± SEM). (B) Flow cytometry of mitochondrial superoxide production in WT and CSB deficient cells after 24 hours treatment with the PARP inhibitors (n=3, mean ± SEM). (C) Whole body oxygen consumption rates in 4 months (young) and 16 months (old) old WT and Csbm/m mice after daily intraperitoneal injections of PJ34 (25mg/kg body weight) (n=3–8, right is the quantification of the slopes). (D) and (E) NAD+ and ATP levels in the cerebellum of young and old WT and Csbm/m mice after 1 week treatment with the NAD+ precursor nicotinamide riboside (n=3–5, mean ± SEM). (F–I) Mebrane potential and ROS production in isolated mitochondria from the cerebellum of WT and Csbm/m mice (n=3–5, mean ± SEM). (J) A principal component analysis and hierarchical clustering of transcriptomic changes in the cerebellum of mice treated with NR. (K) Venn-diagram of significantly changed gene expressions when comparing old Csbm/m saline treated mice vs. old WT saline treated mice and old Csbm/m NR treated mice vs. old WT saline. (L) Venn-diagram of significantly changed gene expressions when comparing old Csbm/m saline treated mice vs. old WT saline treated mice and old Csbm/m NR treated mice vs. old WT saline.