Aim To explore the effects and mechanisms of testosterone on the migratory capacity of bone marrow-derived endothelial progenitor cells （BM-EPC）. Methods BM-EPC were cultured and identified from 6-week-old orchiectomized BALB/C male mice. The adherent cells were collected and divided into eight groups randomly, and cocultured with 0, 1, 10, 100 nmol/L testosterone or corresponding concentration of testosterone and androgen receptors antagonists flutamide. BM-EPC' migration towards stroma cell-derived factor-1α （SDF-1α） was assessed by the method of transwell chamber with or without treatment of chemokine receptor 4 （CXCR4） inhibitor AMD3100, and the CXCR4 expression in BM-EPC was detected by reverse transcription polymerase chain reaction （RT-PCR） and Western blot. BM-EPC'migration was assessed by the method of transwell. Results Compared with control group, the migration towards SDF-1α of BM-EPC was increased by testosterone in a dose-dependent manner （group A: 61.80±9.31 group B: 83.20±6.53 group C: 107.00±12.85 group D: 134.80±8.64 P＜0.05）. The CXCR4 mRNA expression of BM-EPC was increased by testosterone in a dose-dependent manner compared with control group （group A: 0.065±0.005 group B: 0.114±0.002 group C: 0.149±0.019 group D: 0.209±0.013 P＜0.05）. The CXCR4 protein expression of BM-EPC was increased by testosterone in a dose-dependent manner compared with control group （group A: 0.23±0.06 group B: 0.40±0.02 group C: 0.62±0.04 group D: 0.77±0.05 P＜0.05）. However, these effects were blocked by flutamide. Different concentrations of testosterone on the role of BM-EPC migration were blocked by AMD3100. Conclusion Testosterone enhances the migratory capacity of BM-EPC by up-regulating the CXCR4 expression via androgen receptors pathway.