Chinese Journal of Tissue Engineering Research ›› 2024, Vol. 28 ›› Issue (35): 5669-5674.doi: 10.12307/2024.809

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Vascular endothelial growth factor 165/bone morphogenetic protein improves osteoblast injury under hypoxic and reoxygenated conditions

Zhao Yiting1, Zhang Yuxiang2, Ma Jie1, He Xuejiao1   

  1. 1Department of Orthopedics, 2Clinical Laboratory, The Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi 830001, Xinjiang Uygur Autonomous Region, China
  • Received:2023-10-25 Accepted:2023-12-28 Online:2024-12-18 Published:2024-03-15
  • Contact: Zhang Yuxiang, Clinical Laboratory, The Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi 830001, Xinjiang Uygur Autonomous Region, China
  • About author:Zhao Yiting, Associate chief technician, Department of Orthopedics, The Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi 830001, Xinjiang Uygur Autonomous Region, China

Abstract: BACKGROUND: It has been found that vascular endothelial growth factor 165 and bone morphogenetic proteins interact with each other during hypoxia-reoxygenation and are involved in the repair process of osteoblast injury by regulating the activation of intracellular signaling pathways.
OBJECTIVE: To further investigate the relationship between vascular endothelial growth factor 165/bone morphogenetic protein and hypoxic-reoxygenated osteoblast injury. 
METHODS: Osteoblasts were selected and the hypoxic-reoxygenated injury model was established. Vascular endothelial growth factor 165 and bone morphogenetic protein expressions at mRNA and protein levels were detected by real-time PCR and western blot before and after modeling. After modeling, osteoblasts were given different concentrations of vascular endothelial growth factor 165 and bone morphogenetic protein 2 (10, 20, 40 ng/mL). Cell proliferation was detected by cell counting kit-8 method and apoptosis was detected by DAPI at 12, 24, 36, 48, and 72 hours after treatment.
RESULTS AND CONCLUSION: Compared with before modeling, the mRNA and protein expressions of vascular endothelial growth factor 165 and bone morphogenetic protein 2 in osteoblasts after modeling were significantly decreased (P < 0.05). The proliferation rate of osteoblasts was significantly increased with the increase of vascular endothelial growth factor 165 concentration (P < 0.05), while the apoptosis rate of osteoblasts decreased significantly with the increase of vascular endothelial growth factor 165 concentration (P < 0.05). The proliferation rate of osteoblast was significantly increased with the increase of bone morphogenetic protein 2 concentration (P < 0.05), while the apoptosis rate of osteoblast decreased significantly with the increase of bone morphogenetic protein 2 concentration (P < 0.05). To conclude, vascular endothelial growth factor 165 and bone morphogenetic protein are lowly expressed in hypoxic-reoxygenated osteoblast injury, and treatment with vascular endothelial growth factor 165 and bone morphogenetic protein can reduce the injury of hypoxic-reoxygenated osteoblast in a concentration-dependent manner, suggesting that vascular endothelial growth factor 165 and bone morphogenetic protein have a significant protective effect against the injury of hypoxic-reoxygenated osteoblasts.

Key words: vascular endothelial growth factor 165, bone morphogenetic protein 2, hypoxia-reoxygenation, osteoblast, cell apoptosis

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