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首页> 外文期刊>Cell and Tissue Research >Replacing Shox2 with human SHOX leads to congenital disc degeneration of the temporomandibular joint in mice
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Replacing Shox2 with human SHOX leads to congenital disc degeneration of the temporomandibular joint in mice

机译：用人类SHOX替代Shox2会导致小鼠颞下颌关节先天性椎间盘退变

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摘要

The temporomandibular joint (TMJ) consists in the glenoid fossa arising from the otic capsule through intramembranous ossification, the fibrocartilaginous disc and the condyle, which is derived from the secondary cartilage by endochondral ossification. We have reported previously that cranial neural-crest-specific inactivation of the homeobox gene Shox2, which is expressed in the mesenchymal cells of the maxilla-mandibular junction and later in the progenitor cells and perichondrium of the developing chondyle, leads to dysplasia and ankylosis of the TMJ and that replacement of the mouse Shox2 with the human SHOX gene rescues the dysplastic and ankylosis phenotypes but results in a prematurely worn out articular disc. In this study, we investigate the molecular and cellular bases for the prematurely worn out articular disc in the TMJ of mice carrying the human SHOX replacement allele in the Shox2 locus (termed Shox2 SHOX-KI/KI). We find that the developmental process and expression of several key genes in the TMJ of Shox2 SHOX-KI/KI mice are similar to that of controls. However, the disc of the Shox2 SHOX-KI/KI TMJ exhibits a reduced level of Collagen I and Aggrecan, accompanied by increased activities of matrix metalloproteinases and a down-regulation of Ihh expression. Dramatically increased cell apoptosis in the disc was also observed. These combinatory cellular and molecular defects appear to contribute to the observed disc phenotype, suggesting that, although human SHOX can exert similar functions to mouse Shox2 in regulating early TMJ development, it apparently has a distinct function in the regulation of those molecules that are involved in tissue homeostasis.
机译：颞下颌关节（TMJ）由通过膜内骨化，通过art软骨盘和the突形成的耳膜囊从耳囊中产生的盂状窝组成，which突是通过软骨内骨化而形成的。我们以前曾报道过同源异型盒基因Shox2的颅神经neural特异性失活，它在上颌-下颌交界的间充质细胞中表达，然后在发育中的软骨的祖细胞和软骨膜中表达，导致异型增生和关节强直TMJ和用人类SHOX基因替代小鼠Shox2可以挽救发育不良和强直性表型，但会导致关节盘过早磨损。在这项研究中，我们调查了携带人SHOX替代等位基因在Shox2基因座（称为Shox2 SHOX-KI / KI）的小鼠TMJ中过早磨损的关节盘的分子和细胞基础。我们发现Shox2 SHOX-KI / KI小鼠的TMJ的发育过程和几个关键基因的表达与对照相似。但是，Shox2 SHOX-KI / KI TMJ的碟片显示胶原I和Aggrecan的水平降低，同时基质金属蛋白酶的活性增加，Ihh表达下调。还观察到椎间盘中的细胞凋亡显着增加。这些组合的细胞和分子缺陷似乎有助于观察到的椎间盘表型，这表明，尽管人类SHOX在调节早期TMJ发育中可以发挥与小鼠Shox2类似的功能，但显然在调节与这些分子有关的分子中具有独特的功能。组织动态平衡。

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