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Role of hypoxia inducible factor-1α and VHL in murine endochondral ossification 期刊论文

编号：

9229c0ff-6d8b-4f7d-a077-7fb9294b26fc
作者：

Shao, Jin[0];Deng, Lianfu[1];Qi, Jin[2];Zhou, Qi[3];Wang, Jun[4];Wei, Li[5];Wang, Jinshen[6];Qian, Niandong[7];
地址：

Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory for Bone and Joint Diseases,Shanghai,China[0];Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases with Integrated Chinese-Western Medicine,Shanghai,China[1];Shanghai Jiao Tong University School of Medicine, Department of Orthopaedics,Shanghai,China[2];Shanghai Jiao Tong University School of Medicine, Department of Orthopaedics,Shanghai,China[3];Fudan University, Department of Materials Science,Shanghai,China[4];Shanghai Jiaotong University, Department of Endocrinology & Metabolism,Shanghai,China[5];Anhui Medical University, Department of General Surgery,Hefei,China[6];Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases with Integrated Chinese-Western Medicine,Shanghai,China[7];
语种：

中文
期刊：

Journal of Shanghai Jiaotong University (Medical Science) ISSN：1674-8115 2009 年 29 卷 11 期 (1305 - 1310)
收录：
关键词：

Endochondral ossification Hypoxia inducible factor-1α Von Hippel-Lindau
摘要：

Objective: To investigate the role of hypoxia inducible factor-1α (HIF-1α) and von Hippel-Lindau (VHL) in murine endochondral ossification. Methods: The knockout of HIF-1α or VHL gene in murine osteoblasts was accomplished by conditional knockout technique at 4th, 8th and 12th week, and the differences between wild-type group and knock-out group in endochondral ossification were detected by HE staining, micro-CT scanning, trabecular bone area measurement, calcium content measurement, tetracycline fluorescence labeling, Real-time PCR and Western blotting. Results: After knockout of HIF-1α gene in osteoblasts, the expression of vascular endothelial growth factor (VEGF) reduced, the rate of new bone formation stepped down, the content of calcium became less, and the trabecular bone volume decreased (P < 0.05). After knockout of VHL gene in osteoblasts, the expression of VEGF increased, the rate of new bone formation stepped up, the content of calcium became more, and the trabecular bone volume was promoted (P < 0.001). Conclusion: During murine endochondral ossification, VHL/HIF-1α signal pathway promotes angiogenesis through the stimulation of VEGF expression, which subsequently accelerates osteogenesis.
推荐引用方式
GB/T 7714：

Shao Jin[0],Deng Lianfu[1],Qi Jin[2], 等. Role of hypoxia inducible factor-1α and VHL in murine endochondral ossification [J].Journal of Shanghai Jiaotong University (Medical Science),2009,29(11):1305-1310.
APA：

Shao Jin[0],Deng Lianfu[1],Qi Jin[2],Zhou Qi[3],&Qian Niandong[7].(2009).Role of hypoxia inducible factor-1α and VHL in murine endochondral ossification .Journal of Shanghai Jiaotong University (Medical Science),29(11):1305-1310.
MLA：

Shao Jin[0], et al. "Role of hypoxia inducible factor-1α and VHL in murine endochondral ossification" .Journal of Shanghai Jiaotong University (Medical Science) 29,11(2009):1305-1310.

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