Overexpression of Dlx2 leads to postnatal condyle degradation.
Overexpression of Dlx2 leads to postnatal condyle degradation.
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DOI：
10.3892/mmr.2016.5406
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发表时间：
2016-08
影响因子：
3.4
通讯作者：
Shen G
中科院分区：
文献类型：
--
作者：
Dai J;Si J;Zhu X;Zhang L;Wu D;Lu J;Ouyang N;Wang X;Shen G
非远端同源异型盒2（Dlx 2）是Dlx家族转录因子的一员，在颅面组织的发育中起重要作用。先前的研究基于敲除突变小鼠发现，Dlx2主要干扰组织的发育从上颌弓，本研究使用转基因小鼠模型，特异性过表达Dlx2的神经嵴细胞，以探讨Dlx2过表达的作用，在出生后的小鼠髁突。通过大体观察、显微CT扫描和组织学检查观察模型的表型。该模型证实Dlx2过表达可能导致髁突畸形、软骨下骨降解和髁突软骨组织结构不规则。此外，髁突区骨钙素的表达明显下调，而msh同源框2的表达上调。本研究结果提示，Dlx 2在颅神经嵴细胞中的过表达会干扰小鼠生后髁突的发育，表明Dlx 2的表达水平和时空表达模式可能在调节小鼠生后髁突发育中起重要作用，也为今后的研究提供了一种可能的颞下颌关节骨关节炎模型动物。
Distal-less homeobox 2 (Dlx2), a member of the Dlx family of transcription factors, is important for the development of craniofacial tissues. Previous studies based on knock-out mutant mice revealed that Dlx2 primarily disturbed the development of tissues from maxillary arch. The present study used a transgenic mouse model to specifically overexpress Dlx2 in neural crest cells in order to investigate the role of Dlx2 overexpression in post-natal condyle in mice. The model was constructed and the phenotype observed using gross observation, micro-CT scan and histological examination. The model determined that overexpression of Dlx2 may lead to postnatal condyle malformation, subchondral bone degradation and irregular histological structure of the condylar cartilage. In addition, the expression of osteocalcin in the condyle region was markedly downregulated, whereas expression of msh homeobox 2 was upregulated. The results of the present study suggest that Dlx2 overexpression in cranial neural crest cells would disrupt the development of post-natal condyle, which demonstrates that the expression level and the spatiotemporal expression patterns of Dlx2 may be important in regulating the development of post-natal condyle in mice, and also offered a possible temporal-mandibular joint osteoarthritis model animal for future studies.