Upregulated microRNA‐126 induces apoptosis of dental pulp stem cell via mediating PTEN‐regulated Akt activation

Introduction Human dental pulp stem cells (DPSCs) have potential applications in regenerative medicine. The molecular mechanisms underlying DPSCs viability and apoptosis are not completely understood. Here, we investigated the role of miR‐126 in DPSCs viability and apoptosis. Material and methods Senescent DPSCs were compared with early passage DPSCs. real‐time PCR and microARRAY were performed to identify the differential expression of miR‐126, and western blot was performed to detect the expression of PTEN. MTT assay was utilized to reveal the proliferative rate of both senescent and early passage DPSCs. Flow cytometry was used to examine the apoptotic rate of DPSCs. Dual‐luciferase reporter assay was carried out to detect the interaction of miR‐126 and PTEN. Results Senescent DPSCs showed a high level of apoptosis. Further study showed that miR‐126 is upregulated in senescent DPSCs and its overexpression in early passaged DPSCs induced apoptosis. Phosphatase and tensin homolog gene (PTEN) was identified as a target of miR‐126. PTEN was downregulated in senescent DPSCs, whereas miR‐126 inhibition upregulated PTEN level, and subsequently activated Akt pathway and suppressed the apoptotic phenotype of senescent DPSCs. In addition, PTEN overexpression rescued apoptosis of DPSCs at later stage. Conclusion Our results demonstrate that the miR‐126‐PTEN‐Akt axis plays a key role in the regulation of DPSCs apoptosis and provide a candidate target to improve the functional and therapeutic potential of DPSCs. To probe the role of miR‐126 on cell proliferation and apoptosis of early and later DPSC, the cells at PD16 were transfected with miR‐126 mimic or control, while cells at PD54 were transfected with miR‐126 inhibitor or control to regulate the miR‐126 expression. For early DPSC group, data displayed that there was no any influence, while miR‐126 caused a reduced cell proliferative rate. For DPSC at PD54, miR‐126 inhibition significantly increased the cell replication of DPSC during 72 h post transfection. These data suggested that miR‐126 played an inhibitory role in DPSC viability.