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Fig. 3 | The Journal of Physiological Sciences

Fig. 3

From: Mst1 promotes cardiac ischemia–reperfusion injury by inhibiting the ERK-CREB pathway and repressing FUNDC1-mediated mitophagy

Fig. 3

Mst1 deletion protects mitochondria against reperfusion-mediated damage. Cardiomyocytes were isolated from WT mice and Mst1-deleted mice. Then, hypoxia for 30 min and reoxygenation for 2 h were applied in vitro to mimic cardiac I/R injury. Subsequently, mitochondrial function and mitochondrial apoptosis were measured. a, b ROS production was detected via flow cytometry. c, d Mitochondrial potential was observed via JC-1 staining; the normal mitochondria displayed red fluorescence, whereas the damaged mitochondria exhibited green fluorescence. e, f The cellular location of cyt-c was observed via immunofluorescence assay. The nuclear expression of cyt-c was recorded. g–m After H/R injury in vitro, proteins were isolated and western blotting was performed to analyze the expression of proteins related to 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

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