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.
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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
Li C
中科院分区:
医学4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

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颞下颌关节(TMJ)是一种独特的滑膜关节,其发育与其他滑膜关节不同,由两种不同的间充质致密物发育而成,所述间充质致密物朝向彼此生长并通过不同的机制骨化。Shox 2基因在TMJ发育中起重要作用,先前的研究已经证明Shox 2SHOX KI/KI小鼠表现出TMJ缺陷表型、先天性发育不良和关节盘过早侵蚀,这在临床上被定义为TMJ病症。在本研究中,Shox 2SHOX KI/KI小鼠模型被用来研究先天性骨关节炎(OA)样疾病在出生后TMJ生长的机制。观察到Shox 2SHOX KI/KI小鼠从产后第7天起出现严重的肌肉萎缩综合征。组织学检查表明,Shox 2SHOX KI/KI小鼠的髁突和关节窝在出生后第二周的大小减少。Shox 2SHOX KI/KI小鼠的髁突显示II型胶原和印度刺猬蛋白的表达水平降低,而I型胶原的表达增加。髁突中基质金属蛋白酶9(MMP 9)和MMP 13也明显增加。这些细胞和分子缺陷可能导致观察到的Shox 2SHOX KI/KI小鼠TMJ的(OA)样表型。
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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发表时间: 2014-02
影响因子: 7
作者:
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