Figure 4.
Figure 4. Migration of HEK 293 cells in responses to CXCL11. (A) Migration of HEK 293 cells expressing WT CXCR3 receptors toward CXCL11 is PTx dependent. HEK 293-WT CXCR3 cells were preincubated with 100 ng/mL PTx for 2 hours at 37°C and washed prior to assay. Migration was performed as described in “Materials and methods” in response to 50 ng/mL CXCL11. A representative experiment of 3 performed is presented. Each value represents the mean SD of triplicates of the representative experiment. Using ANOVA and the Newman-Keuls test, the difference was significant for PTx/CXCL11 treatment (*P < .05). (B) Migration of HEK 293-CXCR3 was dependent mainly upon the receptor C-tail. Migration of HEK 293 cells expressing the various CXCR3 mutants was performed as described in “Materials and methods” in response to 50 ng/mL CXCL11. Percentage inhibition of migration by each mutant of CXCR3 was calculated as number of migrating cells expressing mutated CXCR3 per HPF versus the number of migrating cells expressing WT CXCR3 per HPF. Each value represents the mean ± SD of inhibition calculated of 3 independent experiments. Using ANOVA, the difference of percentage inhibition between the CXCR3 mutants was significant (*P < .05). Multiple comparisons between the mutants by the Newman-Keuls test showed that only S245A and D37 were different from each other.

Migration of HEK 293 cells in responses to CXCL11. (A) Migration of HEK 293 cells expressing WT CXCR3 receptors toward CXCL11 is PTx dependent. HEK 293-WT CXCR3 cells were preincubated with 100 ng/mL PTx for 2 hours at 37°C and washed prior to assay. Migration was performed as described in “Materials and methods” in response to 50 ng/mL CXCL11. A representative experiment of 3 performed is presented. Each value represents the mean SD of triplicates of the representative experiment. Using ANOVA and the Newman-Keuls test, the difference was significant for PTx/CXCL11 treatment (*P < .05). (B) Migration of HEK 293-CXCR3 was dependent mainly upon the receptor C-tail. Migration of HEK 293 cells expressing the various CXCR3 mutants was performed as described in “Materials and methods” in response to 50 ng/mL CXCL11. Percentage inhibition of migration by each mutant of CXCR3 was calculated as number of migrating cells expressing mutated CXCR3 per HPF versus the number of migrating cells expressing WT CXCR3 per HPF. Each value represents the mean ± SD of inhibition calculated of 3 independent experiments. Using ANOVA, the difference of percentage inhibition between the CXCR3 mutants was significant (*P < .05). Multiple comparisons between the mutants by the Newman-Keuls test showed that only S245A and D37 were different from each other.

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