Fig. 3
From: Mst1 regulates post-infarction cardiac injury through the JNK-Drp1-mitochondrial fission pathway
Mst1 promoted cardiomyocyte death in the heart after a myocardial infarction (MI). a and b The TUNEL assay was used to observe cellular apoptosis in vivo in wild-type (WT) and Mst1-knockout (Mst1KO) cells. c–i The mitochondrial apoptotic proteins pro-caspase-3, cleaved caspase-3 (Cle.caspase-3), caspase-9, Bax, Bad, Bcl2, survivin and β-actin were measured via western blots. Mst1 elevated mitochondrial apoptotic protein levels in the post-infarcted heart. j and k Cardiomyocytes were isolated from WT and Mst1KO mice and a hypoxia model was used to induce cardiomyocyte damage in vitro. The MTT and caspase-3 activity assays were used to assess cellular viability *p < 0.05 vs. sham group, #p < 0.05 vs. WT mice in post-MI group