Figure 1.
Figure 1. HUVECs as a model for TKI-associated vascular toxicity. HUVECs were treated with clinically relevant concentrations of nontoxic imatinib and compared directly to 3 toxic TKIs (dasatinib, ponatinib, and nilotinib). (A-B) Leukocyte adhesion (A) was quantified from representative images (B) of adherent fluorescently labeled U937 leukocytes. (C-D) Wound healing (C) was determined by quantifying the number of HUVECs that migrated into the scratch wound from representative images (D) after 20 hours. (E) HUVEC survival was quantified by the Cell TiterGlo Luminescent assay. Data are presented as mean fold change ± standard error of the mean relative to vehicle-treated control. Significance was determined by 1-way analysis of variance and Dunnett post-test. **P < .01; ***P < .001 vs vehicle. ###P < .001 vs imatinib. The number of experiments per condition is displayed within each bar. (B,D) Original magnification ×4.

HUVECs as a model for TKI-associated vascular toxicity. HUVECs were treated with clinically relevant concentrations of nontoxic imatinib and compared directly to 3 toxic TKIs (dasatinib, ponatinib, and nilotinib). (A-B) Leukocyte adhesion (A) was quantified from representative images (B) of adherent fluorescently labeled U937 leukocytes. (C-D) Wound healing (C) was determined by quantifying the number of HUVECs that migrated into the scratch wound from representative images (D) after 20 hours. (E) HUVEC survival was quantified by the Cell TiterGlo Luminescent assay. Data are presented as mean fold change ± standard error of the mean relative to vehicle-treated control. Significance was determined by 1-way analysis of variance and Dunnett post-test. **P < .01; ***P < .001 vs vehicle. ###P < .001 vs imatinib. The number of experiments per condition is displayed within each bar. (B,D) Original magnification ×4.

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