Figure 6
Figure 6. Ex vivo perfusion of murine carotid arteries with monocytic Monomac 6 cells (MM6). Ad.empty– and Ad.hVEGF-A–treated arteries were perfused with MM6 cells labeled with calcein/AM at a flow rate of 3 μL/min. Some monocytic cells were preincubated with sJAM.Fc, sPECAM-1.Fc, and anti–VLA-4 at 37°C for 30 minutes. Adhesive interactions with the atherosclerotic vessel wall were recorded using epifluorescence illumination and cells not moving for more than 30 seconds were defined as adherent. (A) MM6 cells adhere to Ad.hVEGF-A–treated (bottom panel) and Ad.empty–treated (top panel) carotid arteries after 10 minutes of perfusion. Flow direction from was right to left. (B) Quantification of adherent cells reveals that VEGF-A overexpression led to a significant increase in the adherence of MM6 cells, which could be blocked by pretreatment of MM6 cells with anti–VLA-4 and sPECAM-1.Fc, but not by sJAM.Fc. *P < .05 versus Ad.empty; **P < .05 versus Ad.hVEGF-A. Error bars indicate standard deviation.

Ex vivo perfusion of murine carotid arteries with monocytic Monomac 6 cells (MM6). Ad.empty– and Ad.hVEGF-A–treated arteries were perfused with MM6 cells labeled with calcein/AM at a flow rate of 3 μL/min. Some monocytic cells were preincubated with sJAM.Fc, sPECAM-1.Fc, and anti–VLA-4 at 37°C for 30 minutes. Adhesive interactions with the atherosclerotic vessel wall were recorded using epifluorescence illumination and cells not moving for more than 30 seconds were defined as adherent. (A) MM6 cells adhere to Ad.hVEGF-A–treated (bottom panel) and Ad.empty–treated (top panel) carotid arteries after 10 minutes of perfusion. Flow direction from was right to left. (B) Quantification of adherent cells reveals that VEGF-A overexpression led to a significant increase in the adherence of MM6 cells, which could be blocked by pretreatment of MM6 cells with anti–VLA-4 and sPECAM-1.Fc, but not by sJAM.Fc. *P < .05 versus Ad.empty; **P < .05 versus Ad.hVEGF-A. Error bars indicate standard deviation.

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