Fig. 4
From: Mst1 regulates post-infarction cardiac injury through the JNK-Drp1-mitochondrial fission pathway
Mst1 impacted mitochondrial function and structure. a and b ROS production was higher in response to hypoxia treatment in wild-type cells (WT-cell) but was lower with Mst1 knockout (Mst1KO-cell). c and d The mitochondrial potential was measured via JC-1 staining. e The mPTP opening rate was evaluated and found to be highest in WT cells under conditions of hypoxia. Mst1 knockout meant mPTP opening rates closer to the normal level. f and g The immunofluorescence assay of cyt-c translocation from the cytoplasm (green staining) into the nucleus (blue staining). h Caspase-9 activity was measured to reflect mitochondrial apoptosis. *p < 0.05 vs. ctrl group, #p < 0.05 vs. WT-cell+hypoxia