Fig. 6

Mst1 modulates FUNDC1 via the ERK-CREB pathway. a–d Western blotting was used to analyze the effect of Mst1 deletion on ERK phosphorylation and CREB phosphorylation. Subsequently, to inhibit the ERK activity in Mst1-deleted cardiomyocytes, we added PD98059 to Mst1-deleted cells. Then, the FUNDC1 expression was detected to establish the regulatory effect of ERK on FUNDC1 activation. e Immunofluorescence assay for p-CREB and FUNDC1. Both p-CREB and FUNDC1 expression were significantly inhibited by H/R injury and were reversed to near-normal levels with Mst1 deletion. f, g Caspase-9 activity and LDH release assays were measured to confirm the role of the ERK-CREB pathway in mitochondrial apoptosis. Data are presented as the mean ± SEM. H/R injury hypoxia–reoxygenation injury, WT-cell cardiomyocytes isolated from WT mice, Mst1-KO cell cardiomyocytes isolated from Mst1 knockout mice. *P < 0.05