Figure 1
Figure 1. Effect of the (β15-66)2 fragment on the distribution of VE-cadherin in endothelial cells. (A-F) HUVECs grown on glass coverslips to confluence were incubated for 6 hours without (A-C) or with 250nM (β15-66)2 fragment (D-F), fixed, permeabilized, and immunostained for VE-cadherin (red in panels A and D), actin (green in panels B and E), and nuclei (blue in panels C and F). (G-I) The inhibitory effect of RAP on the (β15-66)2–induced redistribution of VE-cadherin in HUVECs is shown. Cells grown to confluence were incubated for 24 hours with media alone (G), with 250nM (β15-66)2 (H), or with 250nM (β15-66)2 plus 500nM RAP (I), fixed, permeabilized, and immunostained for VE-cadherin. All confocal images were taken through the middle of the cell layer. Magnification ×63, oil immersion.

Effect of the (β15-66)2 fragment on the distribution of VE-cadherin in endothelial cells. (A-F) HUVECs grown on glass coverslips to confluence were incubated for 6 hours without (A-C) or with 250nM (β15-66)2 fragment (D-F), fixed, permeabilized, and immunostained for VE-cadherin (red in panels A and D), actin (green in panels B and E), and nuclei (blue in panels C and F). (G-I) The inhibitory effect of RAP on the (β15-66)2–induced redistribution of VE-cadherin in HUVECs is shown. Cells grown to confluence were incubated for 24 hours with media alone (G), with 250nM (β15-66)2 (H), or with 250nM (β15-66)2 plus 500nM RAP (I), fixed, permeabilized, and immunostained for VE-cadherin. All confocal images were taken through the middle of the cell layer. Magnification ×63, oil immersion.

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