Objective: To evaluate whether EPC-MVs could promote bone regeneration by directly regulating osteoblast through miR-126. The underlying mechanisms were also explored. Methods: EPCs were isolated from bone marrow mononuclear cells. EPC-MVs were collected from EPCs cultured medium. The lentivirus was used to induce miR-126 over-expression in EPCs and EPC-MVs. miR-126 expression was detected by qRT-PCR. The proliferation, migration, apoptosis and differentiation abilities of osteoblast cells MC3T3-E1 were analysed in the presence or absence of EPC-MVs or miR-126 overexpressed EPC-MVs (EPC-MVs-miR126). The proteins of Erk1/2 and Bcl-2 were analysed by western blot. Erk1/2 inhibitor was used for pathway exploration. Results: EPC-MVs reduced apoptosis and promoted proliferation and migration of MC3T3-E1 cells, which could be enhanced by miR-126 enrichment (p< 0.05). Neither EPC-MVs nor EPC-MVs-miR126 had an effect on MC3T3-E1 cell osteogenic differentiation (p> 0.05). EPC-MVs-miR126 had better effects than EPC-MVs on upregulating the expressions of p-Erk1/2 and Bcl-2, which were abolished by Erk1/2 inhibitor. ERK1/2-Bcl-2 activity plays a crucial role in the regulation of EPC-MVs/EPC-MVs-miR126 on the effect of MC3T3-E1 cells. Conclusion: EPC-MVs promote proliferation and migration of MC3T3-E1 cell while reduced apoptosis via the miR-126/Erk1/2-Bcl-2 pathway. A combination of EPC-MVs and miR-126 might provide novel therapeutic targets for bone regeneration and fracture healing through regulating osteoblast.

目的：评价EPC-MVs是否可以通过miR-126直接调节成骨细胞促进骨再生。还探讨了潜在的机制。方法：从骨髓单个核细胞中分离EPC。从EPCs培养基中收集EPC-MV。慢病毒用于诱导EPC和EPC-MV中的miR-126过表达。通过qRT-PCR检测到miR-126表达。在存在或不存在EPC-MV或miR-126过表达的EPC-MV（EPC-MVs-miR126）的情况下分析成骨细胞MC3T3-E1的增殖，迁移，凋亡和分化能力。通过蛋白质印迹分析Erk1 / 2和Bcl-2的蛋白质。Erk1 / 2抑制剂被用于途径探索。结果：EPC-MVs减少凋亡并促进MC3T3-E1细胞的增殖和迁移，这可以通过miR-126富集来增强（p <0.05）。EPC-MV和EPC-MVs-miR126均不影响MC3T3-E1细胞的成骨分化（p > 0.05）。EPC-MVs-miR126在上调prk-Erk1 / 2和Bcl-2的表达方面优于EPC-MV，后者被Erk1 / 2抑制剂取消。ERK1 / 2-Bcl-2活性在调节EPC-MVs / EPC-MVs-miR126对MC3T3-E1细胞的作用中起着至关重要的作用。结论：EPC-MVs通过miR-126 / Erk1 / 2-Bcl-2途径促进MC3T3-E1细胞的增殖和迁移，同时减少细胞凋亡。EPC-MV和miR-126的组合可能通过调节成骨细胞为骨再生和骨折愈合提供新的治疗靶标。