Replacing Shox2 with human SHOX leads to congenital disc degeneration of the temporomandibular joint in mice

Li, Xihai; Liu, Hongbing; Gu, Shaohua; Liu, Chao; Sun, Cheng; Zheng, Yanhui

doi:10.1007/s00441-013-1743-2

Cited by 17 publications

(35 citation statements)

References 51 publications

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“…Results demonstrated that the number of apoptotic cells increased dramatically in the SHOX2 silencing group compared to control, suggesting that SHOX2 was involved in the regualtion of NP cell apoptosis. This is similar to a previous study, which found that the number of apoptotic cells increased dramatically in articular disc of SHOX2 SHOX‐KI/KI TMJ …”

Section: Discussionsupporting

confidence: 92%

“…It has been reported that pMes‐stop SHOX2 in TMJ resulted in reduction of Col I, Col II, AGG, and Gli2, along with increased cell apoptosis, as well as enhanced MMPs (MMP9 and MMP13) activity in the condyle . Li et al also reported that the expression of collagen I decreased in the SHOX2 SHOX‐KI/KI TMJ disc, aggrecan decreased in the disc and condoyle of SHOX2 SHOX‐KI/KI TMJ. Furthermore, they found that MMP9 and MMP13 expression was enhanced in the articular disc of SHOX2 SHOX‐KI/KI TMJ.…”

Section: Discussionmentioning

confidence: 95%

“…Previous studies have demonstrated that over-expression of SHOX2 in the heart results in abnormal cardiac formation 29 and inactivation of SHOX2 leads to abnormal development of the TMJ. 30 A SHOX2 knock-out resulted in a complete absence of chondrocyte maturation and a marked decrease in chondrocyte proliferation. 22 NP consists of small chondrocyte-like cells with typical morphology 25 that share a common developmental lineage with cartilage at molecular level.…”

Section: Discussionmentioning

confidence: 99%

“…number of apoptotic cells increased dramatically in articular disc of SHOX2 SHOX-KI/KI TMJ. 30 Relevant to cell proliferation, previous studies have demonstrated that the impact of SHOX2 on proliferation was cell-specific. The regulation of SHOX2 on NP cell proliferation was evaluated, results showed that SHOX2 inhibition by siRNA led to decreased proliferation of NP cells.…”

Section: Role Of Shox2 In the Development Of Intervertebralmentioning

confidence: 99%

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Role of SHOX2 in the development of intervertebral disc degeneration

Wang

Zheng

et al. 2017

J. Orthop. Res.

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Intervertebral disc (IVD) degeneration is the most common cause of low back pain, which affect 80% of the population during their lives, with heavy economic burden. Many factors have been demonstrated to participate in IVD degeneration. In this study, we investigated the role of short stature homeobox 2 (SHOX2) in the development of IVD degeneration. First, we detected the expression of SHOX2 in different stages of human IVD degeneration; then explored the role of SHOX2 on nucleus pulposus (NP) cells proliferation and apoptosis, finally we evaluated the effect of SHOX2 on the production of extracellular matrix in NP cells. Results showed that the expression of SHOX2 is mainly in NP compared with AF tissues, its expression decreased with the severity of human IVD degeneration. TNF-α treatment led to dose- and time-dependent decrease in SHOX2 mRNA, protein expression and promoter activity in NP cells. The silencing of SHOX2 inhibited NP cells proliferation and induced NP cells apoptosis. Finally, SHOX2 silencing led to decreased aggrecan and collagen II expression, along with increased ECM degrading enzymes MMP3 and ADAMTS-5 in NP cells. In summary, our results indicated that SHOX2 plays an important role in the process of IVD degeneration, and might be a protective factor for IVD degeneration. Further studies are required to confirm its exact role, and clarify the mechanism. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1047-1057, 2017.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Section: Role Of Shox2 In the Development Of Intervertebralmentioning

confidence: 99%

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Role of SHOX2 in the development of intervertebral disc degeneration

Wang

Zheng

et al. 2017

J. Orthop. Res.

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“…A number of transcription factors and growth factors have been reported with regard to their essential roles in TMJ morphogenesis and growth, such as Runx2, Sox9, Shox2, Spry1 and Spry2, Bmpr1A, Tgfbr2, and Ndst1 (Shibata et al 2004; Fukuoka et al 2007; Mori-Akiyama et al 2003; Wang et al 2011; Gu et al 2008, 2014; Li et al 2014; Purcell et al 2012; Oka et al 2007; Yasuda et al 2010). Among them, Indian hedgehog (Ihh), a signaling molecule that plays a pivotal role in the regulation of chondrocyte proliferation, maturation, and ossification both in long-bone development and digit joint formation (St-Jacques et al 1999), has also been found to be essential for TMJ development (Shibukawa et al 2007; Purcell et al 2009; Gu et al 2014).…”

Section: Introductionmentioning

confidence: 99%

Augmented Indian hedgehog signaling in cranial neural crest cells leads to craniofacial abnormalities and dysplastic temporomandibular joint in mice

Yang

et al. 2015

Cell Tissue Res

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Extensive studies have pinpointed the crucial role of Indian hedgehog (Ihh) signaling in the development of the appendicular skeleton and the essential function of Ihh in the formation of the temporomandibular joint (TMJ). In this study, we have investigated the effect of augmented Ihh signaling in TMJ development. We took a transgenic gain-of-function approach by overexpressing Ihh in the cranial neural crest (CNC) cells using a conditional Ihh transgenic allele and the Wnt1-Cre allele. We found that Wnt1-Cre-mediated tissue-specific overexpression of Ihh in the CNC lineage caused severe craniofacial abnormalities, including cleft lip/palate, encephalocele, anophthalmos, micrognathia, and defective TMJ development. In the mutant TMJ, the glenoid fossa was completely absent, whereas the condyle and the articular disc appeared relatively normal with slightly delayed chondrocyte differentiation. Our findings thus demonstrate that augmented Ihh signaling is detrimental to craniofacial development, and that finely tuned Ihh signaling is critical for TMJ formation. Our results also provide additional evidence that the development of the condyle and articular disc is independent of the glenoid fossa.

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Transcriptomic and proteomic studies of condylar ossification of the temporomandibular joint in porcine embryos

Xiang,

Li,

Wang

et al. 2023

Anim Models and Exp Med

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BackgroundThe ossification mechanism of the temporomandibular joint (TMJ) condyle remains unclear in human embryo. The size and structure of TMJ, shape of articular disc and the characteristics of omnivorous chewing in the pig are similar to those of humans. The pig is an ideal animal for studying the mechanism of ossification of the TMJ condyle during the embryonic period.MethodIn a previous study by our group, it was found that there was no condylar ossification on embryonic day(E) 45, but the ossification of condyle occurred between E75 and E90. In this study, a total of 12 miniature pig embryos on E45 and E85 were used. Six embryos were used for tissue sections (3 in each group). The remaining six embryos were used for transcriptomic and proteomic studies to find differential genes and proteins. The differentially expressed genes in transcriptome and proteomic analysis were verified by QPCR.ResultsIn total, 1592 differential genes comprising 1086 up‐regulated genes and 506 down‐regulated genes were screened for fold changes of ≥2 to ≤0.5 between E45 and E85. In the total of 4613 proteins detected by proteomic analysis, there were 419 differential proteins including 313 up‐regulated proteins and 106 down‐regulated proteins screened for fold changes of ≥2 to ≤0.5 between E45 and E85. A total of 36 differential genes differing in both transcriptome and proteome analysis were found. QPCR analysis showed that 14 of 15 selected genes were consistent with transcriptome analysis.ConclusionCondylar transcriptome and proteomic analysis during the development of TMJ in miniature pigs revealed the regulatory genes/proteins of condylar ossification.

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Replacing Shox2 with human SHOX leads to congenital disc degeneration of the temporomandibular joint in mice

Cited by 17 publications

References 51 publications

Role of SHOX2 in the development of intervertebral disc degeneration

Role of SHOX2 in the development of intervertebral disc degeneration

Augmented Indian hedgehog signaling in cranial neural crest cells leads to craniofacial abnormalities and dysplastic temporomandibular joint in mice

Transcriptomic and proteomic studies of condylar ossification of the temporomandibular joint in porcine embryos

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