Figure 7
Figure 7. Comparison of integrin activation in WT and kindlin-2+/− aortic endothelial cells. (A) Dose-dependence of soluble Alexa 488–labeled Fg binding to resting or PMA-stimulated ECs. Soluble Fg binding to kindlin-2+/− ECs is decreased and independent on PMA stimulation. (B) Soluble Fg (50 μg/mL) binding to WT and kindlin-2+/− ECs in the presence of VEGF and Mn2+ ions. Fg binding to kindlin-2+/− ECs is significantly reduced and independent on VEGF stimulation. (C) Soluble FITC-collagen I (50 μg/mL) binding to WT and kindlin-2+/− ECs in the presence of VEGF and Mn2+ ions. Collagen I binding to WT and kindlin-2+/− ECs is the same in the absence or presence of VEGF. All data are means ± SEM of triplicate samples and are representative of 3 independent experiments with pooled ECs from 4-6 mice.

Comparison of integrin activation in WT and kindlin-2+/− aortic endothelial cells. (A) Dose-dependence of soluble Alexa 488–labeled Fg binding to resting or PMA-stimulated ECs. Soluble Fg binding to kindlin-2+/− ECs is decreased and independent on PMA stimulation. (B) Soluble Fg (50 μg/mL) binding to WT and kindlin-2+/− ECs in the presence of VEGF and Mn2+ ions. Fg binding to kindlin-2+/− ECs is significantly reduced and independent on VEGF stimulation. (C) Soluble FITC-collagen I (50 μg/mL) binding to WT and kindlin-2+/− ECs in the presence of VEGF and Mn2+ ions. Collagen I binding to WT and kindlin-2+/− ECs is the same in the absence or presence of VEGF. All data are means ± SEM of triplicate samples and are representative of 3 independent experiments with pooled ECs from 4-6 mice.

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