Fig. 1.

MST1 upregulation mediates cardiomyocyte cytotoxicity in response to DOX in vitro, a–b MST1 expression profile after two and four hours of treatment with 50 μM of doxorubicin in primary cardiomyocyte cultures. Densitometric data normalized by loading control represent mean ± SEM (n = 7 independent samples); c–d P-LATS and LATS expression profiles after two and four hours of treatment with 50 μM of doxorubicin. Densitometric data normalized by loading control and expressed as P-LATS/LATS ratio ± SEM (n = 5 independent samples); e–f TUNEL (green) staining of cardiomyocyte cultures infected with ad-LacZ or ad-DN-MST1 for 48 h, and then treated with doxorubicin (50 μM) for four hours. Nuclei were counterstained with DAPI. Data represent mean ± SEM (n = 4 independent samples). Scale bar = 200 μm; g Cl-Caspase 3 protein profile from cardiomyocyte cultures infected with ad-LacZ or ad-DN-MST1 for 48 h, then treated with doxorubicin (50 μM) for four hours. Representative images of five independent experiments; h MTS colorimetric assay of cardiomyocyte cultures infected with ad-LacZ or ad-DN-MST1 for 48 h and then treated with doxorubicin (50 μM) for 24 h. Data represent mean ± SEM (n = 11 independent samples). Data were analysed with a two-tailed Student’s t-test (b, d) or one-way ANOVA with Bonferroni post-hoc test (f–h). *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001; ****P ≤ 0.0001; ns = not significant (P > 0.05)