Figure 1
Figure 1. Expression of CXCL12 receptors, CXCR4 and CXCR7, in blood monocytes and contribution to CXCL12 mediated-chemotaxis. (A) CXCR4 and CXCR7 immunofluorescence of blood monocytes from 2 different donors (top and middle panels), and the THP-1 monocytic cell line (bottom panel). Unpermeabilized (membrane, left and middle) and permeabilized (total, right) cells were analyzed by flow cytometry. (B) Monocytes were pretreated with the CXCR4 antagonist (AMD3100; 25 μg/mL), with the CXCR7 antagonist (CCX733; 100nM) or with anti-CXCR4/CXCR7 antibodies (50 μg/mL) and allowed to migrate to CXCL12. Untreated (−) cells were used as migration control (100%). CXCL12-induced chemotaxis of CXCR7 siRNA-transfected THP-1 cells was compared with control siRNA-transfected cells. The percentages of migration referred to CXCL12-mediated chemotaxis are shown. Mean ± SD; n = 3; *P < .05, **P < .005, ***P < .0005.

Expression of CXCL12 receptors, CXCR4 and CXCR7, in blood monocytes and contribution to CXCL12 mediated-chemotaxis. (A) CXCR4 and CXCR7 immunofluorescence of blood monocytes from 2 different donors (top and middle panels), and the THP-1 monocytic cell line (bottom panel). Unpermeabilized (membrane, left and middle) and permeabilized (total, right) cells were analyzed by flow cytometry. (B) Monocytes were pretreated with the CXCR4 antagonist (AMD3100; 25 μg/mL), with the CXCR7 antagonist (CCX733; 100nM) or with anti-CXCR4/CXCR7 antibodies (50 μg/mL) and allowed to migrate to CXCL12. Untreated (−) cells were used as migration control (100%). CXCL12-induced chemotaxis of CXCR7 siRNA-transfected THP-1 cells was compared with control siRNA-transfected cells. The percentages of migration referred to CXCL12-mediated chemotaxis are shown. Mean ± SD; n = 3; *P < .05, **P < .005, ***P < .0005.

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