Fig. 2: Partial loss of SLC25A51 impairs liver regeneration and mildly decreases mitochondrial respiratory capacity.
From: Hepatocyte mitochondrial NAD+ content is limiting for liver regeneration
Male Slc25a51+/− mice and wild-type littermates were subjected to two thirds PHx and analysed 48 h later. a, A schematic of the experimental design. b, The representative sections of regenerating livers stained with H&E. The mitotic figures are marked by black arrows. c,d, The liver-to-body-weight ratios (n = 15 for A51+/+ and n = 14 for A51+/−) (c) and mitotic index (n = 9 for A51+/+ and n = 10 for A51+/−) (d) at 48 h post PHx. e,f, The hepatic TG (e) and ATP (f) content pre and 48 h post hepatectomy (n = 9 for pre in both genotypes; n = 7 for A51+/+ TG and n = 5 for A51+/+ ATP post PHx; n = 8 for A51+/− TG and n = 8 for A51+/− ATP post PHx). g,h, The hepatic NAD+ (g) and liver mitochondrial NAD+ (h) content pre and 48 h post injury (n = 9 for pre in both genotypes; n = 8 for A51+/+ liver and n = 7 for A51+/+ mito post PHx; n = 6 for A51+/− for both liver and mito post PHx). i–k, The oxygen consumption flux in isolated mitochondria from resected (n = 6 for all groups) (i) and regenerated livers (n = 7 for all groups) (j) using complex I (CI, pyruvate), complex II (CII, succinate) and complex IV (CIV, TMPD-ASC)-dependent substrates or palmitoyl carnitine to measure fatty acid oxidation (FAO) (k) in A51 heterozygous mice and wild-type littermates (n = 5 for pre and n = 7 for post in both genotypes). The data are presented as the mean, and the error bars represent s.e.m. The ANOVA results are shown as main effects of genotype ($), time ($) and interaction (&). The individual P values are shown where significant (P ≤ 0.05). The tests for normality and equality of variances, along with the resulting statistical test selected for each panel, are provided in the statistical source data. 10HPF, ten high-power fields; O2 flux(mt), mitochondrial oxygen consumption flux.
