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. 2015 May 25;107(1):66–77. doi: 10.1093/cvr/cvv152

Figure 1.

Figure 1

TKIs induce cardiotoxicity and cell death in NRVMs. (A) Fetal gene expression was measured in NRVMs treated with 150 ng/mL Sunitinib for 36 h using quantitative PCR. Fold change is relative to vehicle-treated. ANF, atrial natriuretic factor; BNP, brain natriuretic peptide; β-MyHC, β-myosin heavy chain; α-SkActin, α-Skeletal actin. n = 4 NRVM preparations analysed separately. Bars indicate the average fold change of the four preparations. Student's t-test, comparing Sunitinib- to vehicle-treated cells. (B) Absorbance at 590 nm (A590) of crystal violet-stained NRVMs treated with vehicle (DMSO), 75 ng/mL, 150 ng/mL, or 300 ng/mL Sunitinib (Sun) for 36 h. n = 6 NRVM preparations analysed separately. Bars indicate the average of the six preparations. One-way ANOVA followed by Tukey's post-hoc test. (C) Fold change in caspase-3 activity measured in lysates from NRVMs treated with 150 ng/mL Sunitinib for 24, 48, 72, 96, or 120 h. n = 3 NRVM preparations of 80–100 neonatal ventricles each. One-way ANOVA followed by Tukey's post-hoc test. For each panel, error bars represent standard error from the mean (SEM). *P < 0.05, **P < 0.01.