Objective      To determine the effect of CXCL12 on the proliferation of rat oligodendrocyte precursor cells (OPCs)  and explore the related mechanism.       Methods      OPCs were dissociated by shaking process and differential adhesion

and identified by immunocytochemical assay. The effect of different concentrations (0

5

10 and 20 ng/mL) of CXCL12 on the proliferation of OPCs at 0

24

48

and 72 h was assessed by CCK-8 assay

and the expression levels of downstream CXCR4

CXCR7 and MMP9 at 72 h were detected by Western blotting. CXCR4 siRNA and CXCR7 siRNA were used to inhibit CXCR4 and CXCR7 expression

respectively. Then

the effect of 20 ng/mL CXCL12 on the proliferation of OPCs was assessed by CCK-8 assay

and the expression levels of downstream CXCR4

CXCR7 and MMP9 at 72 h were detected by Western blotting. MMP9 siRNA was used to inhibit MMP9 expression

and the effect of 20 ng/mL CXCL12 on proliferation of OPCs was assessed by CCK-8 assay.       Results      Certain concentration range of CXCL12 significantly promoted the proliferation of OPCs

and enhanced the expression levels of CXCR4

CXCR7 and MMP9. Compared with 0 ng/mL CXCL12

20 ng/mL CXCL12 treatment for 72 h significantly promoted the proliferation of OPCs and the expression levels of CXCR4

CXCR7 and MMP9 (P0.05). After inhibiting CXCR4 and CXCR7 expression

the proliferation of OPCs was inhibited

and the MMP9 expression was also significantly reduced (P0.05). After inhibiting MMP9 expression

the proliferation of OPCs was inhibited (P0.05).       Conclusion      CXCL12 can significantly promote the proliferation of OPCs through promoting CXCR4

CXCR7 and MMP9 expression

which provides an experimental foundation for OPCs transplantation therapy of spinal cord injury (SCI).