Fig. 1 | Nature Communications

Fig. 1

From: The mitochondrial negative regulator MCJ is a therapeutic target for acetaminophen-induced liver injury

Fig. 1

MCJ expression determines the susceptibility of hepatocytes to APAP toxicity. a, b Cell death in WT and MCJ KO hepatocytes using TUNEL assay (a) and Trypan blue staining (b) after treatment with APAP for 9 and 6 h, respectively. c JNK activation was evaluated by western blotting in WT and MCJ KO hepatocytes after APAP exposure. d, e Cell death in MCJ KO hepatocytes and MCJ KO hepatocytes transfected with MCJ (MCJ KO-MCJ) using TUNEL assay (d) and Trypan blue staining (e) after treatment with APAP for 9 and 6 h, respectively. f, g Cell death in WT hepatocytes and WT hepatocytes transfected with siMCJ (siMCJ) using TUNEL assay (f) and Trypan blue staining (g) after treatment with APAP for 9 and 6 h, respectively. hj Mitochondrial ROS in WT and MCJ KO hepatocytes (h), MCJ KO hepatocytes, and MCJ KO hepatocytes transfected with MCJ (i), WT hepatocytes, and WT hepatocytes transfected with siMCJ (j) MCJ KO-MCJ upon 6 h of APAP treatment using MitoSOX staining. Values are represented as mean ± SEM. *P < 0.05 (Student’s t test) (MCJ KO vs. WT, MCJ KO-MCJ vs. MCJ KO, and siMCJ vs. WT). Triplicates were used for experimental condition