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血管内皮生长因子及其在长骨骨骺早期发育中的作用。

VEGF and its role in the early development of the long bone epiphysis.

机构信息

Department of Anatomy, Histology and Embryology, Division of Clinical and Functional Anatomy, Innsbruck Medical University, Innsbruck, Austria.

出版信息

J Anat. 2010 May;216(5):611-24. doi: 10.1111/j.1469-7580.2010.01223.x.

Abstract

In long bones of murine species, undisturbed development of the epiphysis depends on the generation of vascularized cartilage canals shortly after birth. Despite its importance, it is still under discussion how this event is exactly regulated. It was suggested previously that, following increased hypoxia in the epiphyseal core, angiogenic factors are expressed and hence stimulate the ingrowth of the vascularized canals. In the present study, we tested this model and examined the spatio-temporal distribution of two angiogenic molecules during early development in mice. In addition, we investigated the onset of cartilage hypertrophy and mineralization. Our results provide evidence that the vascular endothelial growth factor is expressed in the epiphyseal resting cartilage prior to the moment of canal formation and is continuously expressed until the establishment of a large secondary ossification centre. Interestingly, we found no expression of secretoneurin before the establishment of the canals although this factor attracts blood vessels under hypoxic conditions. Epiphyseal development further involves maturation of the resting chondrocytes into hypertrophic ones, associated with the mineralization of the cartilage matrix and eventual death of the latter cells. Our results suggest that vascular endothelial growth factor is the critical molecule for the generation of the epiphyseal vascular network in mice long bones. Secretoneurin, however, does not appear to be a player in this event. Hypertrophic chondrocytes undergo cell death by a mechanism interpreted as chondroptosis.

摘要

在鼠类长骨中,骺软骨的正常发育依赖于出生后不久血管化软骨管的生成。尽管这一事件非常重要,但它的确切调控机制仍存在争议。先前有研究表明,骺核缺氧增加后,血管生成因子被表达,从而刺激血管化管的生长。在本研究中,我们检验了这一模型,并检测了两种血管生成分子在早期发育过程中的时空分布。此外,我们还研究了软骨肥大和矿化的起始。我们的研究结果表明,血管内皮生长因子在形成管腔之前就已经在骺软骨静止区表达,并持续表达,直到形成大的次级骨化中心。有趣的是,尽管分泌素原在缺氧条件下吸引血管生成,但我们在管腔形成之前没有发现它的表达。骺的进一步发育还涉及静止软骨细胞向肥大软骨细胞的成熟,伴随着软骨基质的矿化和后者细胞的最终死亡。我们的结果表明,血管内皮生长因子是小鼠长骨骺血管网络生成的关键分子。然而,分泌素原似乎不是这一事件的参与者。肥大软骨细胞通过一种被解释为软骨细胞凋亡的机制发生细胞死亡。

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