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Fig. 1 | The Journal of Physiological Sciences

Fig. 1

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

Fig. 1

Mst1 is upregulated by cardiac I/R injury and contributes to myocardial damage and expansion of the infarct area. a, b Cardiac I/R injury was induced via 30 min of ischemia and 2 h of reperfusion in WT mice and Mst1-knockout (Mst1-KO) mice. Then, heart tissues were isolated and western blotting was used to analyze the Mst1 expression before and after cardiac I/R injury. c and e TTC and Evans blue staining were used to analyze the infarction area. The white area in the heart section indicates the infarcted zone. d, f After cardiac I/R injury, a TUNEL assay was carried out to observe cardiomyocyte death. The TUNEL-positive cells detected by TUNEL manifesting brown nuclei were apoptotic cells. g An electron microscope was used to observe the ultrastructure of infarcted hearts. h–k After cardiac I/R injury, heart tissues were isolated and western blotting was performed to detect the levels of inflammation. MMP9, TNFα and IL-8 were increased in response to I/R injury and were reduced to near-normal levels with Mst1 deletion. l The activity of MMP9 was measured via ELISA. MMP9 matrix metalloproteinase 9, TNFα tumor necrosis factor alpha, IL-8 interleukin 8. Data are presented as the mean ± SEM (n = 6, for each group). I/R injury ischemia–reperfusion injury. *P < 0.05

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