Fig. 6.
Fig. 6. Altered in vivo leukocyte rolling in ST3Gal-IVΔ/Δ mice during TNF-α–induced vascular inflammation. / (A) Leukocyte rolling per 100 μm vessel segment length was assessed in ST3Gal-IVΔ/Δ mice (▪) and control mice (░) treated with either P-selectin blocking mAb RB40.34 or E-selectin blocking mAb 9A9. Data are presented as the mean ± SEM. * indicates significant difference; P < .05. (B-D) Cumulative velocity distribution for ST3Gal-IVΔ/Δ mice (solid line) and wild-type littermates (dotted line) with (B) no treatment, (C) P-selectin blocking mAb RB40.34, and (D) E-selectin blocking mAb 9A9. Significant differences in leukocyte velocity (*P < .05) between ST3Gal-IVΔ/Δ mice and wild-type mice were observed for anti–P-selectin–treated mice and mice without antibody treatment, indicating an E-selectin ligand defect.

Altered in vivo leukocyte rolling in ST3Gal-IVΔ/Δ mice during TNF-α–induced vascular inflammation.

(A) Leukocyte rolling per 100 μm vessel segment length was assessed in ST3Gal-IVΔ/Δ mice (▪) and control mice (░) treated with either P-selectin blocking mAb RB40.34 or E-selectin blocking mAb 9A9. Data are presented as the mean ± SEM. * indicates significant difference; P < .05. (B-D) Cumulative velocity distribution for ST3Gal-IVΔ/Δ mice (solid line) and wild-type littermates (dotted line) with (B) no treatment, (C) P-selectin blocking mAb RB40.34, and (D) E-selectin blocking mAb 9A9. Significant differences in leukocyte velocity (*P < .05) between ST3Gal-IVΔ/Δ mice and wild-type mice were observed for anti–P-selectin–treated mice and mice without antibody treatment, indicating an E-selectin ligand defect.

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