Expressing human SHOX in Shox2SHOX KI/KI mice leads to congenital osteoarthritis‑like disease of the temporomandibular joint in postnatal mice.
Expressing human SHOX in Shox2SHOX KI/KI mice leads to congenital osteoarthritis‑like disease of the temporomandibular joint in postnatal mice.
复制标题
在 Shox2(SHOX KI)/(KI) 小鼠中表达人 SHOX 会导致出生后小鼠颞下颌关节先天性骨关节炎样疾病
DOI:
10.3892/mmr.2016.5715
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发表时间:
2016-10
影响因子:
3.4
通讯作者:
Li C
中科院分区:
文献类型:
--
作者:
Liang W;Li X;Chen H;Shao X;Lin X;Shen J;Ding S;Kang J;Li C
The temporomandibular joint (TMJ), a unique synovial joint whose development differs from that of other synovial joints, develops from two distinct mesenchymal condensations that grow toward each other and ossify through different mechanisms. The short stature homeobox 2 (Shox2) gene serves an important role in TMJ development and previous studies have demonstrated that Shox2SHOX KI/KI mice display a TMJ defective phenotype, congenital dysplasia and premature eroding of the articular disc, which is clinically defined as a TMJ disorder. In the present study, Shox2SHOX KI/KI mouse models were used to investigate the mechanisms of congenital osteoarthritis (OA)-like disease during postnatal TMJ growth. Shox2SHOX KI/KI mice were observed to develop a severe muscle wasting syndrome from day 7 postnatal. Histological examination indicated that the condyle and glenoid fossa of Shox2SHOX KI/KI mice was reduced in size in the second week after birth. The condyles of Shox2SHOX KI/KI mice exhibited reduced expression levels of collagen type II and Indian hedgehog, and increased expression of collagen type I. A marked increase in matrix metalloproteinase 9 (MMP9) and MMP13 in the condyles was also observed. These cellular and molecular defects may contribute to the observed (OA)-like phenotype of Shox2SHOX KI/KI mouse TMJs.
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影响因子:
7
作者:
Liu, Y. -D.;Liao, L. -F.;Zhang, H. -Y.;Lu, L.;Jiao, K.;Zhang, M.;Zhang, J.;He, J. -J.;Wu, Y. -P.;Chen, D.;Wang, M. -Q.
通讯作者:
Wang, M. -Q.
影响因子:
7.6
作者:
Ochiai T;Shibukawa Y;Nagayama M;Mundy C;Yasuda T;Okabe T;Shimono K;Kanyama M;Hasegawa H;Maeda Y;Lanske B;Pacifici M;Koyama E
通讯作者:
Koyama E
影响因子:
5.6
作者:
Li X;Liang W;Ye H;Weng X;Liu F;Liu X
通讯作者:
Liu X
影响因子:
2.5
作者:
Wang, Ying;Liu, Chao;Rohr, Joseph;Liu, Hongbing;He, Fenglei;Yu, Jian;Sun, Cheng;Li, Lu;Gu, Shuping;Chen, YiPing
通讯作者:
Chen, YiPing
影响因子:
7
作者:
Rogart, JN;Barrach, HJ;Chichester, CO
通讯作者:
Chichester, CO