Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib

Figure 5

Mitochondrial membrane potential expressed as JC-1 aggregate to monomer ratio in mouse-derived 32D BCR-ABL1+ cells sensitive to imatinib (S) and cells with imatinib resistance resulted from the Y253H mutation in the BCR-ABL1 gene (253) or acquired imatinib resistance (AR) (a). The cells were exposed at 37°C for 24 h to doxorubicin (DOX) at 1 µM (black bars) or unexposed (control, empty bars). Each experiment was repeated four times and error bars denote SD. Numbers indicate significant p values for comparison between pairs connected by brackets. Fluorescent microscopy images of control (untreated) cells and cells treated with 1 µM DOX (b). Red fluorescence of JC-1 dimers is present in the cell areas with high mitochondrial membrane potential, while green fluorescence of JC-monomers is prevalent in the cell areas with low mitochondrial membrane potential. The JC-1 stained cells were visualized under an Olympus inverted fluorescence microscope, model IX70 (Olympus, Tokyo, Japan) with 400x magnification.

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