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Bone fracture is accompanied with poor oxygen supply and nutrient deficiency in the local fracture site, and oxygen supply is an important factor that can affect fracture healing. Hypoxia-inducible factor-1 (HIF-1) plays a key role in the regulation of oxygen homeostasis. HIF-1α is rapidly upregulated in response to hypoxia and antagonizes hypoxia-induced apoptosis. In the present study, the viability of an osteoblast cell line, MC3T3-E1, and the expression of HIF-1α protein in the MC3T3-E1 cells was examined under hypoxic conditions. The HIF-1α level was then manipulated and the reduction in the viability of the MC3T3-E1 cells in response to the hypoxia was re-evaluated. In addition, the regulation of HIF-1α in the adaptation of MC3T3-E1 cells to hypoxia was explored. The results showed that the viability of MC3T3-E1 cells decreased and the expression of HIF-1α protein increased under hypoxic conditions. Furthermore, the reduction in the viability of MC3T3-E1 cells post-hypoxia was attenuated by HIF-1α overexpression, while HIF-1α-knockdown by small interfering RNA enhanced the hypoxia-induced decrease in cell viability. It was additionally found that the forced expression of HIF-1α inhibited the hypoxia-induced cell apoptosis. These findings indicate that the forced expression of HIF-1α inhibits hypoxia-induced apoptosis and thus attenuates the hypoxia-induced decrease in cell viability.

Hypoxia-inducible factor-1α antagonizes the hypoxia-mediated osteoblast cell viability reduction by inhibiting apoptosis