Role of hypoxia inducible factor-1α and VHL in murine endochondral ossification
- VernacularTitle:低氧诱导因子-1α和VHL对小鼠软骨内成骨过程的调控机制
- Author:
Jin SHAO
;
Lianfu DENG
;
Jin QI
;
Qi ZHOU
;
Jun WANG
;
Li WEI
;
Jinshen WANG
;
Niandong QIAN
- Publication Type:Journal Article
- Keywords:
hypoxia inducible factor-1α;
von Hippel-Lindau;
endochondral ossification
- From:
Journal of Shanghai Jiaotong University(Medical Science)
2009;29(11):1305-1310
- CountryChina
- Language:Chinese
-
Abstract:
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.
