Figure 5
Figure 5. Cholesterol depletion suppresses bradykinin-induced filopodia formation. (A) HUVEC invasion in the presence of increasing concentrations of the cholesterol depleting agent M-β-CD (0.15%-2%, 0.5 hours). (B) Effects on internalization of 3H-bradykinin in HUVECs depleted of cholesterol with M-β-CD (MβCD; 2%, 0.5 hours) or depleted with M-β-CD then replenished with cholesterol (CH; 20 μg/mL, 3 hours) in the presence of the CD13 antagonists bestatin (100 μg/mL) or MY7 antibody (CD13 mAb; 1:100 dilution). (C) Effects on bradykinin-induced filopodia formation in HUVECs depleted of cholesterol with M-β-CD or depleted with M-β-CD and replenished with cholesterol in the presence of bestatin (100 μg/mL) or MY7 antibody (CD13 mAb; 1:100 dilution) Data are shown as means (± SD, n = 3).

Cholesterol depletion suppresses bradykinin-induced filopodia formation. (A) HUVEC invasion in the presence of increasing concentrations of the cholesterol depleting agent M-β-CD (0.15%-2%, 0.5 hours). (B) Effects on internalization of 3H-bradykinin in HUVECs depleted of cholesterol with M-β-CD (MβCD; 2%, 0.5 hours) or depleted with M-β-CD then replenished with cholesterol (CH; 20 μg/mL, 3 hours) in the presence of the CD13 antagonists bestatin (100 μg/mL) or MY7 antibody (CD13 mAb; 1:100 dilution). (C) Effects on bradykinin-induced filopodia formation in HUVECs depleted of cholesterol with M-β-CD or depleted with M-β-CD and replenished with cholesterol in the presence of bestatin (100 μg/mL) or MY7 antibody (CD13 mAb; 1:100 dilution) Data are shown as means (± SD, n = 3).

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