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ADAM10 modulates SOX9 expression via N1ICD during chondrogenesis at the cranial base

机译：ADAM10在颅底软骨形成过程中通过N1ICD调节SOX9表达

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The cranial base is the foundation of the craniofacial structure, and any interruption of the cranial base can lead to facial deformity. The cranial base develops from two synchondroses via endochondral ossification. Chondrogenesis is an important step in endochondral ossification. A disintegrin and metalloprotease (ADAM) 10 participates in the Notch1 signalling pathway, which has been reported to regulate chondrogenesis via a SOX9-dependent mechanism. However, little is known about the function of ADAM10 in chondrogenesis. In this study, adam10-conditional-knockout (cKO) mice exhibited sharper naso-labial angles and flatter skulls than wild-type (WT) mice. In the sagittal plane, SOX9 was more widespread in the cranial base in Adam10-cKO mice than in WT mice. For in vitro experiments, we used the ATDC5 cell line as a model to investigate the role of ADAM10 in chondrogenesis. Plasmid 129 was designed to decrease the expression of Adam10; the resulting downregulation of Adam10 reduced the production of N1ICD. Plasmid 129 increased the expression of SOX9 under chondrogenic induction, and this increase could be inhibited by transfection with exogenous N1ICD. Collectively, these results show that ADAM10 participates in chondrogenesis by negatively regulating SOX9 expression in an N1ICD-dependent manner during cranial base development.
机译：颅底是颅面结构的基础，任何颅底断裂都会导致面部畸形。颅底由软骨内骨化从两个软骨融合形成。软骨形成是软骨内骨化的重要步骤。 Disintegrin和金属蛋白酶（ADAM）10参与Notch1信号传导途径，据报道该途径通过SOX9依赖性机制调节软骨形成。但是，关于ADAM10在软骨形成中的功能了解甚少。在这项研究中，与野生型（WT）小鼠相比，adam10-条件敲除（cKO）小鼠的鼻唇唇角和颅骨扁平。在矢状面中，与野生型小鼠相比，Adam10-cKO小鼠的颅底SOX9分布更广。对于体外实验，我们使用ATDC5细胞系作为模型来研究ADAM10在软骨形成中的作用。设计质粒129以减少Adam10的表达。结果，Adam10的下调减少了N1ICD的产生。质粒129在软骨诱导下增加了SOX9的表达，这种增加可以通过用外源性N1ICD转染来抑制。总体而言，这些结果表明，ADAM10通过在颅底发育过程中以N1ICD依赖性方式负调控SOX9的表达来参与软骨形成。

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