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HIF-1α-induced microRNA-210 reduces hypoxia-induced osteoblast MG-63 cell apoptosis
1a Orthopaedics Department , Renmin Hospital of Wuhan University , Wuhan , China.
Abstract:
To better understand the ischemic-hypoxia-induced fracture healing impairment, we determined in this study the microRNA-210 expression in broken bone specimens and in osteoblasts under hypoxia and then determined the influence of microRNA-210 overexpression on the osteoblast cell proliferation and apoptosis. Results demonstrated that microRNA-210 expression was upregulated with an association with HIF-1α overexpression in clinical human catagmatic tissues and was upregulated HIF-1α-dependently in response to hypoxia in osteoblast MG-63 cells. CCK-8 assay indicated that microRNA-210 upregulation by microRNA-210 mimics reduced the chemotherapeutic 5-FU-induced osteoblast cell death, and colony formation assay demonstrated that microRNA-210 mimics promoted osteoblast cells growth. Moreover, the microRNA-210 mimics transfection inhibited the hypoxia-induced MG-63 cell apoptosis via inhibiting the activation of caspase 3 and caspase 9. Therefore, our research indicated a protective role of microRNA-210 in response to hypoxia. And microRNA-210 might serve as a protective role in bone fracture healing.
Insights
MicroRNA-210 protects osteoblasts from hypoxia-induced damage, promoting cell growth and inhibiting apoptosis. This suggests microRNA-210 plays a vital role in fracture healing under ischemic conditions.
Area of Science:
- Biomedical Science
- Molecular Biology
- Orthopedics
Background:
- Ischemic-hypoxia impairs fracture healing.
- MicroRNA-210 (miR-210) role in hypoxia is not fully understood.
- Osteoblast function is critical for bone repair.
Purpose of the Study:
- Investigate miR-210 expression in hypoxia-induced fracture healing impairment.
- Determine the effect of miR-210 overexpression on osteoblast proliferation and apoptosis.
Main Methods:
- Analysis of miR-210 and HIF-1α in clinical bone samples and MG-63 cells.
- Hypoxia exposure of osteoblast cell cultures.
- Overexpression of miR-210 using mimics.
- Cell proliferation assessed by CCK-8 assay.
- Apoptosis evaluated by caspase 3 and 9 activation.
Main Results:
- miR-210 and HIF-1α were upregulated in clinical fracture tissues and hypoxia-exposed osteoblasts.
- miR-210 overexpression reduced chemotherapy-induced cell death and promoted osteoblast growth.
- miR-210 inhibited hypoxia-induced osteoblast apoptosis by suppressing caspase activation.
Conclusions:
- miR-210 exhibits a protective effect against hypoxia in osteoblasts.
- miR-210 upregulation is HIF-1α-dependent.
- miR-210 may play a protective role in fracture healing, especially under hypoxic conditions.
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