HIF-1α protects osteoblasts from ROS-induced apoptosis

The regulatory mechanism of hypoxia-inducible factor-1 alpha (HIF-1 alpha) is complex. HIF-1 alpha may inhibit or promote apoptosis in osteoblasts under different physiological conditions, and induce bone regeneration and repair injury in coordination with angiogenesis. The relationship between H2O2 and HIFs is complex, and this study aimed to explore the role of HIF-1 alpha in H2O2-induced apoptosis. Dimethyloxallyl glycine (DMOG) and 2-Methoxyestradiol (2ME) were used to stabilize and inhibit HIFs, respectively. Cell viability was assessed with CCK8. Apoptosis and ROS levels were detected by flow cytometry, and HIF mRNA expression was assessed by reverse transcription-polymerase chain reaction (RT-PCR). Western blot was performed to detect HIF-1 alpha, HIF-2 alpha, Bax, Bak, Bcl-2, Bcl-XL, caspase-9, and PCNA protein amounts. Our data suggest that both HIF-1 alpha and HIF-2 alpha play a protective role in oxidative stress. HIF-1 alpha reduces H2O2-induced apoptosis by upregulating Bcl-2 and Bcl-XL, downregulating Bax, Bak, and caspase-9, stabilizing intracellular ROS levels, and promoting the repair of H2O2--induced DNA damage to reduce apoptosis.

Automated summary

Both HIF-1α and HIF-2α have a protective role in oxidative stress-induced apoptosis by regulating apoptosis-related proteins and stabilizing ROS levels.