Figure 6
Figure 6. Ang-2-induced leukocyte adhesion. Leukocyte-endothelial interactions of rhodamine-6G–labeled leukocytes in Ang-2 DT and WT littermates were assessed by fluorescence intravital microscopy using the skinfold chamber model (top). (A) Inflammatory activation was induced by superfusion with TNF-α for 2 hours (bottom). (B) The number of rolling cells was not significantly altered by Ang-2 expression. Quantification of adherent leukocytes (arrowheads) revealed significantly increased baseline adhesion in Ang-2 DT mice (n = 4) compared with WT (n = 5). After 2 hours of TNF-α stimulation, the number of adhesive leukocytes further increased above adhesion levels determined in WT mice (C). Data are mean ± SD of 4 animals. Adhesion under shear of CD14+ human monocytes to ICAM-1 was significantly increased when cells were additionally exposed to Ang-2 (cocoating with ICAM-1) compared with BSA control (D). SDF-1α served as a positive control (D). This effect was completely abolished on incubation with an inhibitory antibody against β2-integrin (anti-CD18) but not with control IgG (E). Data are mean ± SEM of 10 independent experiments (using anti-β2 antibody: n = 4). **P < .01. ***P < .005.

Ang-2-induced leukocyte adhesion. Leukocyte-endothelial interactions of rhodamine-6G–labeled leukocytes in Ang-2 DT and WT littermates were assessed by fluorescence intravital microscopy using the skinfold chamber model (top). (A) Inflammatory activation was induced by superfusion with TNF-α for 2 hours (bottom). (B) The number of rolling cells was not significantly altered by Ang-2 expression. Quantification of adherent leukocytes (arrowheads) revealed significantly increased baseline adhesion in Ang-2 DT mice (n = 4) compared with WT (n = 5). After 2 hours of TNF-α stimulation, the number of adhesive leukocytes further increased above adhesion levels determined in WT mice (C). Data are mean ± SD of 4 animals. Adhesion under shear of CD14+ human monocytes to ICAM-1 was significantly increased when cells were additionally exposed to Ang-2 (cocoating with ICAM-1) compared with BSA control (D). SDF-1α served as a positive control (D). This effect was completely abolished on incubation with an inhibitory antibody against β2-integrin (anti-CD18) but not with control IgG (E). Data are mean ± SEM of 10 independent experiments (using anti-β2 antibody: n = 4). **P < .01. ***P < .005.

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