Fig. 5

Glucocorticoid regulated the colocalization of FPR and CXCR4 of bone marrow-derived endothelial progenitor cells. a Colocalization of FPR and CXCR4 in EPCs after double immunofluorescence staining, deconvolution, and spotted treatment. b 2D histogram of Pearson’s coefficient in colocalized volume in EPCs. c Scatterplot of the vesicle relative position of FPR and CXCR4 after vantage treatment in EPCs. Pearson’s coefficient in colocalized volume was significantly increased in EPCs after 75 ng/ml corticosterone treatment (P < 0.05). When pretreated with RU486 (10 μm), Pearson’s coefficient in the colocalized volume of corticosterone-treated EPCs was obviously reversed compared to the GC group. Meanwhile, it was also reversed when pretreated with Cyc H (1 μm), a specific FPR antagonist, and more than that in the GC + RU486 group. *P < 0.05 vs. the 0 ng/ml GC group, ^##P < 0.01 vs. the 75 ng/ml group, ^$$P < 0.01 vs. the 75 ng/ml + 10 μM RU486 group. Data are one of three representative observations