MiR-708 inhibits MC3T3-E1 cells against H(2)O(2)-induced apoptosis through targeting PTEN

BACKGROUND: The dysregulation of proliferation and apoptosis plays a significant role in the pathogenesis of postmenopausal osteoporosis (PO). MicroRNAs play an important role in regulating apoptosis of MC3T3-E1 cells. However, the role and potential mechanism of miR-708 for regulating H(2)O(2)-induced apoptosis is unknown. This study aimed to investigate the protective function of miR-708 in H(2)O(2)-induced apoptosis of MC3T3-E1 osteoblasts. METHODS: MC3T3-E1 was co-cultured with H(2)O(2) for 8 h, then, flow cytometry, malondialdehyde (MDA), and glutathione peroxidase (Gpx) levels were measured to establish the oxidative model. MiRNA microarray was performed to assess differentially expressed miRNAs between control and H(2)O(2)-treated MC3T3-E1 cells. We then performed RT-PCR to identify the relative expression of miR-708 and PTEN. After transfected MC3T3-E1 with miR-708 mimics, flow cytometry, MDA, and Gpx level were performed to identify the apoptosis rate and oxidative stress in these groups. Furthermore, we small interfering RNA of PTEN to identify the role of PTEN in H(2)O(2)-induced apoptosis of MC3T3-E1 cells. RESULTS: H(2)O(2) (100 nM) could significantly induce the apoptosis of MC3T3-E1 cells. Moreover, H(2)O(2) could significantly increase the MDA level and downregulated Gpx level. RT-PCR found that H(2)O(2) significantly decrease the level of miR-708. Compared with H(2)O(2) group, H(2)O(2) + miR-708 mimic significantly decreased the apoptosis rate. CONCLUSIONS: miR-708 plays a protective role in H(2)O(2)-induced MC3T3-E1 osteoblasts apoptosis and its protective effect is proceeded by regulating ROS level and PTEN expression level.