Disruption of MAP7D1 Gene Function Increases the Risk of Doxorubicin-Induced Cardiomyopathy and Heart Failure

Figure 2

Disruption of map7d1b gene in the GBT239 homozygous mutant exacerbated doxorubicin-induced cardiac dysfunction and heart failure. (a) Shown are examples of echocardiography images extracted from movies of beating hearts in WT controls and GBT239/map7d1b homozygous (map7d1b^-/-) mutants at systole (upper panel) and diastole (lower panel) contraction. (b) Quantification of cardiac function indices of ejection fraction (EF) and fractional shortening (FS) measured by echocardiography in the map7d1b^-/- mutant compared to WT control at 4 weeks postdoxorubicin injection. -8, Student’s -test. (c) Representative images of H&E staining of the ventricles at 4 weeks postdoxorubicin injection. Scale bar: 100 μm. (d) Quantification of trabecular muscle density in the map7d1b^-/- mutant compared to WT controls at 4 weeks postdoxorubicin injection. , Student’s -test. (e) Maximum swimming speed of the map7d1b^-/- mutant compared with the WT control at both baseline and 28 days postdoxorubicin injection (dpi). , Student’s -test. (f) Kaplan-Meier survival curves of WT and map7d1b^-/- mutant zebrafish injected with a single bolus of 20 μg/gram body mass (gbm). The map7d1b^-/- mutant had a significantly reduced survival than WT controls. –20, log rank test.

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