Figure 3
From: The Role of Autophagy in Critical Illness-induced Liver Damage
Effect of hepatic autophagy inactivation on markers of hepatic mitochondrial content, mitochondrial biogenesis and mitochondrial oxidative stress in critically ill mice. Hepatic protein expression of NDUFB8, a subunit of mitochondrial complex I (a), ATP5A, a subunit of mitochondrial complex V (b), hepatic mtDNA content (c), hepatic protein expression of TFAM (d), hepatic mRNA expression of pgc1α (e), nrf1 (f), tfam (g), all markers of mitochondrial biogenesis, and the ratio of sod2 mRNA expression over sod1 mRNA expression, a marker of mitochondrial oxidative stress (h) are shown for healthy pair-fed WT mice (white box plots), healthy pair-fed KO mice (dotted box plots), critically ill WT mice (gray box plots) and critically ill KO mice (hatched box plots) at day 1 and day 3. Box plots depict medians with interquartile ranges (IQR) and whiskers are drawn to the furthest point within 1.5 × IQR from the box. n = 10–16 per group. NDUFB8: NADH dehydrogenase 1 beta subcomplex subunit 8; ATP5A: ATP synthase subunit alpha; mtDNA: mitochondrial deoxyribonucleic acid; sod1: superoxide dismutase-1; sod2: superoxide dismutase-2; pgc1α: peroxisome proliferator-activated receptor gamma coactivator 1-alpha; nrf1: nuclear respiratory factor 1; tfam, TFAM: mitochondrial transcription factor A; rn18s: 18 S ribosomal RNA. KO: Mx1-Cre + Atg7 F/F mouse; WT: Mx1-Cre − Atg7 F/F mouse.
