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MiR-708 inhibits MC3T3-E1 cells against H2O2-induced apoptosis through targeting PTEN
Wei Zhang1, Sheng-Yu Cui2, Hong Yi2
1Department of Orthopedics, The Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou, 215004, Jiangsu, China.
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 H2O2-induced apoptosis is unknown. This study aimed to investigate the protective function of miR-708 in H2O2-induced apoptosis of MC3T3-E1 osteoblasts.
Methods:
MC3T3-E1 was co-cultured with H2O2 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 H2O2-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 H2O2-induced apoptosis of MC3T3-E1 cells.
Results:
H2O2 (100 nM) could significantly induce the apoptosis of MC3T3-E1 cells. Moreover, H2O2 could significantly increase the MDA level and downregulated Gpx level. RT-PCR found that H2O2 significantly decrease the level of miR-708. Compared with H2O2 group, H2O2 + miR-708 mimic significantly decreased the apoptosis rate.
Conclusions:
miR-708 plays a protective role in H2O2-induced MC3T3-E1 osteoblasts apoptosis and its protective effect is proceeded by regulating ROS level and PTEN expression level.
Insights
MicroRNA-708 (miR-708) protects osteoblasts from oxidative stress by reducing apoptosis. This finding offers potential therapeutic targets for postmenopausal osteoporosis by regulating reactive oxygen species (ROS) and PTEN expression.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Dysregulated proliferation and apoptosis are key in postmenopausal osteoporosis pathogenesis.
- MicroRNAs regulate apoptosis in MC3T3-E1 cells, but miR-708's role in H2O2-induced apoptosis is unclear.
- This study investigates miR-708's protective function in H2O2-induced osteoblast apoptosis.
Purpose of the Study:
- To investigate the protective role of miR-708 in hydrogen peroxide (H2O2)-induced apoptosis of MC3T3-E1 osteoblasts.
- To elucidate the underlying mechanism involving reactive oxygen species (ROS) and PTEN expression.
Main Methods:
- MC3T3-E1 cells were exposed to H2O2 to establish an oxidative stress model.
- Flow cytometry, malondialdehyde (MDA), and glutathione peroxidase (Gpx) assays assessed apoptosis and oxidative stress.
- MiRNA microarray, RT-PCR, and transfection with miR-708 mimics and PTEN small interfering RNA were employed.
Main Results:
- H2O2 significantly induced MC3T3-E1 cell apoptosis, increased MDA levels, and decreased Gpx levels.
- H2O2 treatment significantly downregulated miR-708 expression.
- Overexpression of miR-708 via mimics reduced H2O2-induced apoptosis rates.
Conclusions:
- miR-708 exhibits a protective effect against H2O2-induced apoptosis in MC3T3-E1 osteoblasts.
- This protective role is mediated by the regulation of reactive oxygen species (ROS) levels.
- miR-708 also influences apoptosis by regulating PTEN expression levels.
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