Figure 5
From: PGC-1β maintains mitochondrial metabolism and restrains inflammatory gene expression
Succinate accumulates in PGC-1β-deficient DCs. (a) Schematic of glucose metabolism and TCA cycle. DCs were transduced with control shRNA or Ppargc1b shRNA and (b) fractional enrichment of select glucose-derived TCA cycle metabolites was measured following culture with U-[13C]-glucose for 6 h. (c) Relative abundance of metabolites were measured by LC–MS (aconitate, α-KG, and succinate) or GC–MS (citrate and malate). (d) Ratio of succinate to malate from measurements in (c). (e) Ratio of succinate to α-KG from measurements in (c). (f) Mitochondria imaged by transmission electron microscopy (dark dots are microbeads used for sorting). (g) Heat maps of the expression of genes from the TCA cycle (left) and cristae formation (right) Reactome pathways. (h) Select inflammatory and metabolic Reactome pathways that are significantly enriched in PGC-1β-deficient versus control DCs. Data from (b–e) are of one experiment representative of two experiments (s.e.m. of three replicates). Statistical analysis in (b) was determined by 2-way ANOVA and represents the comparison of the 13C-labeled fraction between each condition. Statistical significance for (c–e) was determined by unpaired t-test. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
