Replacing Shox2 with human SHOX leads to congenital disc degeneration of the temporomandibular joint in mice.
Replacing Shox2 with human SHOX leads to congenital disc degeneration of the temporomandibular joint in mice.
复制标题
用人类SHOX代替SHOX2会导致小鼠颞下颌关节的先天性椎间盘变性。
DOI：
10.1007/s00441-013-1743-2
复制
发表时间：
2014-02
影响因子：
3.6
通讯作者：
Chen, YiPing
中科院分区：
文献类型：
--
作者：
Li, Xihai;Liu, Hongbing;Gu, Shuping;Liu, Chao;Sun, Cheng;Zheng, Yuqian;Chen, YiPing
The temporomandibular joint (TMJ) consists of the glenoid fossa arising from the otic capsule through intramembranous ossification, the fibrocartilaginous disc and the condyle, 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 maxilla-mandibular junction and later in the progenitor cells and perichondrium of the developing chondyle, led to dysplasia and ankylosis of the TMJ, and replacement of the mouse Shox2 with the human SHOX gene rescued the dysplastic and ankylosis phenotypes but developed a prematurely worn out articular disc. In this study, we investigated the molecular and cellular bases for the premature wear out articular disc in the TMJ of mice carrying the human SHOX replacement allele in the Shox2 locus (referred as Shox2SHOX-KI/KI). We found that the developmental process and expression of several key genes in the TMJ of Shox2SHOX-KI/KI mice appeared similar to the controls. However, the disc of the Shox2SHOX-KI/KI TMJ exhibited a reduced level of Col I and Aggrecan, accompanied by increased activities of matrix metalloproteinases (MMPs) 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 while the human SHOX can exert similar function as the 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.
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影响因子：
1.9
作者：
Kubota, T;Kubota, E;Sato, S
通讯作者：
Sato, S
DOI：
10.1016/j.ijom.2012.03.006
发表时间：
2012-06-01
影响因子：
2.4
作者：
Krisjane, Z.;Urtane, I.;Ragovska, I.
通讯作者：
Ragovska, I.
影响因子：
3.5
作者：
Clement-Jones, M;Schiller, S;Rappold, GA
通讯作者：
Rappold, GA
影响因子：
3
作者：
Kondoh, T;Hamada, Y;Seto, K
通讯作者：
Seto, K
影响因子：
3
作者：
Landesberg, R;Takeuchi, E;Puzas, JE
通讯作者：
Puzas, JE