Figure 2
Figure 2. CD13 regulates bradykinin-induced invasion and internalization, but not its binding to endothelial cells. (A) Effects of increasing concentrations of bradykinin (in serum-free medium containing growth factor supplement) on endothelial invasion. (B) Sensitivity of bradykinin-induced invasion (12.5 μM; ■) to CD13 inhibition by bestatin (100 μg/mL) or MY7 antibody (CD13 mAb, 1:100 dilution) or inhibition of bradykinin signaling by the B2R antagonist HOE140 (10 μM). (C) Binding of 3H-bradykinin to HUVECs at 0°C in the presence or absence of bestatin. (D) Effects of CD13 inhibition by bestatin (100 μg/mL) or MY7 antibody (CD13 mAb, 1:100 dilution) on 3H-bradykinin (50 nM) internalization at 37°C. Data are shown as mean (± SD, n = 3).

CD13 regulates bradykinin-induced invasion and internalization, but not its binding to endothelial cells. (A) Effects of increasing concentrations of bradykinin (in serum-free medium containing growth factor supplement) on endothelial invasion. (B) Sensitivity of bradykinin-induced invasion (12.5 μM; ■) to CD13 inhibition by bestatin (100 μg/mL) or MY7 antibody (CD13 mAb, 1:100 dilution) or inhibition of bradykinin signaling by the B2R antagonist HOE140 (10 μM). (C) Binding of 3H-bradykinin to HUVECs at 0°C in the presence or absence of bestatin. (D) Effects of CD13 inhibition by bestatin (100 μg/mL) or MY7 antibody (CD13 mAb, 1:100 dilution) on 3H-bradykinin (50 nM) internalization at 37°C. Data are shown as mean (± SD, n = 3).

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