Fig. 7.
Fig. 7. SDF-1–induced chemotaxis of HEK/CD4.403 cells stably transfected with wild-type or mutated CXCR4 molecules. / Cells were subjected to chemotaxis by using SDF-1α at 65, 125, or 250 nM, fixed, stained, and counted under a high-power field microscope. (A) Migration index obtained with the different clones (⋄, CXCR4−; ●, CXCR4+; ■, CXCR4.ICL1m; ○, CXCR4.ICL2m; ▴, CXCR4.ICL2mDRY; ▪, CXCR4.ICL3m; ▵, CXCR4.7TM). Results are expressed as means of at least 5 independent experiments; error bars reflect SDs. (B) Inhibition of SDF-1–induced chemotaxis in HEK/CD4.403/CXCR4 cells. Cells expressing wild-type CXCR4 were preincubated overnight with PTX (100 ng/mL). SDF-1 was also added to the upper and lower chemotaxis chambers (250 nM) to eliminate the chemokine gradient. Data are expressed as means ± SDs of 3 independent experiments. Statistical analysis was performed as described in “Materials and methods” (*P < .05, **P < .01, ***P < .001).

SDF-1–induced chemotaxis of HEK/CD4.403 cells stably transfected with wild-type or mutated CXCR4 molecules.

Cells were subjected to chemotaxis by using SDF-1α at 65, 125, or 250 nM, fixed, stained, and counted under a high-power field microscope. (A) Migration index obtained with the different clones (⋄, CXCR4; ●, CXCR4+; ■, CXCR4.ICL1m; ○, CXCR4.ICL2m; ▴, CXCR4.ICL2mDRY; ▪, CXCR4.ICL3m; ▵, CXCR4.7TM). Results are expressed as means of at least 5 independent experiments; error bars reflect SDs. (B) Inhibition of SDF-1–induced chemotaxis in HEK/CD4.403/CXCR4 cells. Cells expressing wild-type CXCR4 were preincubated overnight with PTX (100 ng/mL). SDF-1 was also added to the upper and lower chemotaxis chambers (250 nM) to eliminate the chemokine gradient. Data are expressed as means ± SDs of 3 independent experiments. Statistical analysis was performed as described in “Materials and methods” (*P < .05, **P < .01, ***P < .001).

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