Fig. 7: DEX-enhanced apoptosis is dependent on mitochondria-derived ROS production and could be rescued by BMP4 pre-treatment. | Cell Death & Disease

Fig. 7: DEX-enhanced apoptosis is dependent on mitochondria-derived ROS production and could be rescued by BMP4 pre-treatment.

From: The detrimental effects of glucocorticoids exposure during pregnancy on offspring’s cardiac functions mediated by hypermethylation of bone morphogenetic protein-4

Fig. 7

Mitochondrial membrane potential (ΔΨm) was detected by JC-1 staining. When the mitochondrial membrane is intact, the JC-1 dye accumulates in mitochondria matrix and emits a red signal. When the mitochondrial membranes are damaged, the JC-1 dye diffuses into the cytoplasm and emits a green signal. a The myocardiocytes manifested significant increase in green fluorescence intensity after H/R from prenatally DEX-exposed offspring, compared with the prenatally NS-exposed control. This depletion of ΔΨm can be inhibited by the pre-treatment of BMP4 24 h prior to H/R. b The ratio of red absorbency vs green was quantified by a multifunction microplate reader. c ATP level, another indicator for mitochondrial functions, was significantly lower in the cardiomyocytes undergone H/R from rats prenatally exposed to DEX than those exposed to NS, and was restored by BMP4 pre-treatment. d, e Mito-SOX staining showed that the production of ROS was elevated in cardiomyocytes undergone H/R from rats prenatally exposed to DEX compared with those exposed to NS, and was significantly reversed in the presence of BMP4 prior to H/R. Data shown are mean ± SEM. *p < 0.05, **p < 0.01; #p < 0.05, ##p < 0.01 compared with prenatally DEX-exposed male offspring

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