Figure 6.
Figure 6. CD177-mediated ERK activation impairs chemoreceptor signaling. (A) Neutrophils were pretreated with MEK inhibitor U0126 (1 µM, 15 min), exposed to αCD177, and then allowed to migrate through a 3-µm pore transwell toward LTB4 for 2 h. ERK inhibition partially rescued migration from CD177 ligation-mediated blockade. (B) Neutrophils were preincubated with αCD177 or isotype (10 µg/mL, 10 min RT) and allowed to migrate across 3- µm transwells for 2 h in response to increasing doses of LTB4. (C) Neutrophils were loaded with the Ca2+-sensitive dye Fluo4 and stimulated with LTB4 ± preincubation with U0126 (1 µM, 15 min), demonstrating suppression of Ca2+ flux by CD177 ligation. Each experiment is representative of at least 2 replicates. Means ± SEMs. *P < .05; **P < .01; ***P < .001; ****P < .0001; by 1-way ANOVA (A) or 2-way ANOVA (B-C).

CD177-mediated ERK activation impairs chemoreceptor signaling. (A) Neutrophils were pretreated with MEK inhibitor U0126 (1 µM, 15 min), exposed to αCD177, and then allowed to migrate through a 3-µm pore transwell toward LTB4 for 2 h. ERK inhibition partially rescued migration from CD177 ligation-mediated blockade. (B) Neutrophils were preincubated with αCD177 or isotype (10 µg/mL, 10 min RT) and allowed to migrate across 3- µm transwells for 2 h in response to increasing doses of LTB4. (C) Neutrophils were loaded with the Ca2+-sensitive dye Fluo4 and stimulated with LTB4 ± preincubation with U0126 (1 µM, 15 min), demonstrating suppression of Ca2+ flux by CD177 ligation. Each experiment is representative of at least 2 replicates. Means ± SEMs. *P < .05; **P < .01; ***P < .001; ****P < .0001; by 1-way ANOVA (A) or 2-way ANOVA (B-C).

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