Figure 2
Figure 2. Chemotaxis and actin polymerization in primary MCL cells in response to CXCL12 and CXCL13. (A) Actin polymerization of MCL cells in response to CXCL12 and CXCL13. Intracellular F-actin content in MCL cells was determined at the time points indicated on the horizontal axis after the addition of 200 ng/mL CXCL12 or CXCL13. Inhibition of CXCL12-induced actin polymerization was detected after preincubation with Plerixafor or pertussis toxin. The relative F-actin content compared with samples before chemokine stimulation (100%) is displayed on the vertical axis and is the mean plus or minus SEM of 4 MCL samples from different patients. (B) Effect of Plerixafor on actin polymerization in response to CXCL12 stimulation. Remarkable inhibition of actin changes mediated by CXCL12 was demonstrated after pretreatment with Plerixafor. The histograms show representative results from one of 4 experiments with MCL B cells from different patients. (C) Displayed is the mean relative chemotaxis of primary MCL cells toward the chemokines CXCL12 or CXCL13 under the conditions displayed on the vertical axis. MCL cells display relatively high levels of spontaneous migration toward wells without chemokine (control). CXCL12 and CXCL13 both induced chemotaxis of MCL cells, and CXCL12-induced chemotaxis is inhibited by pretreatment with pertussis toxin or Plerixafor. Results are percentages of migrated cells relative to input and are mean ± SEM of 4 experiments. *Significant difference compared with control sample (P < .05).

Chemotaxis and actin polymerization in primary MCL cells in response to CXCL12 and CXCL13. (A) Actin polymerization of MCL cells in response to CXCL12 and CXCL13. Intracellular F-actin content in MCL cells was determined at the time points indicated on the horizontal axis after the addition of 200 ng/mL CXCL12 or CXCL13. Inhibition of CXCL12-induced actin polymerization was detected after preincubation with Plerixafor or pertussis toxin. The relative F-actin content compared with samples before chemokine stimulation (100%) is displayed on the vertical axis and is the mean plus or minus SEM of 4 MCL samples from different patients. (B) Effect of Plerixafor on actin polymerization in response to CXCL12 stimulation. Remarkable inhibition of actin changes mediated by CXCL12 was demonstrated after pretreatment with Plerixafor. The histograms show representative results from one of 4 experiments with MCL B cells from different patients. (C) Displayed is the mean relative chemotaxis of primary MCL cells toward the chemokines CXCL12 or CXCL13 under the conditions displayed on the vertical axis. MCL cells display relatively high levels of spontaneous migration toward wells without chemokine (control). CXCL12 and CXCL13 both induced chemotaxis of MCL cells, and CXCL12-induced chemotaxis is inhibited by pretreatment with pertussis toxin or Plerixafor. Results are percentages of migrated cells relative to input and are mean ± SEM of 4 experiments. *Significant difference compared with control sample (P < .05).

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