[No authors listed]
The migration of endogenous neural stem cells and neural precursor cells (NPCs) to sites of injury is essential for neuroregeneration following hypoxicâischemic events. Bone marrowâderived mesenchymal stem cells (BMSCs) are a potential therapeutic source of cells following central nervous system damage; however, few studies have investigated the effects of BMSCs on cell migration. Thus, in the present study, the effects of BMSCs on NPC migration were investigated. In the present study, BMSCs and NPCs were isolated and cultured from mice. The effects of BMSCs on the migration of NPCs were analyzed using a Transwell cell migration assay. BMSCs were transfected with microRNAâ210 (miRâ210) mimics and inhibitors to examine the effects of the respective upregulation and downregulation of miRâ210 in BMSCs on the migration of NPCs. Then, miRâ210 expression in BMSCs were quantified and the expression levels of vascular endothelial growth factorâC (VEGFâC), brain derived neurotrophic factor (BDNF) and chemokine CâC motif ligand 3 (CCL3) in the supernatant under hypoxic conditions were investigated via reverse transcriptionâquantitative polymerase chain reaction (RTâqPCR) and ELISA. Subsequently, the expression of VEGFâC, BDNF and CCL3 in BMSCs overexpressing miRâ210 or BMSCs suppressing miRâ210 was examined by RTâqPCR and western blot analyses. BMSCs promoted the migration of NPC, particularly when preâcultured with BMSCs for 24Â h and coâcultured with NPCs for 24Â h; the miRâ210 expression levels increased under hypoxic conditions. Additionally, the migration of NPCs was also increased when the BMSCs overexpressed miRâ210 compared with the BMSCs transfected with a negative control miR and BMSCs with downregulated miRâ210 levels. The expression levels of VEGFâC increased in the BMSCs that overexpressed miRâ210 and were decreased in BMSCs transfected with a miRâ210 inhibitor. The results of the present study indicated that BMSCs promote the migration of NPCs. Overexpression of miRâ210 in BMSCs enhanced NPC migration and may be associated with increases in VEGFâC expression levels.
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