Tissue interaction is required for glenoid fossa development during temporomandibular joint formation

Wang, Ying; Liu, Chao; Rohr, Joseph; Liu, Hongbing; He, Fenglei; Yu, Jian; Sun, Cheng; Lü, Li; Gu, Shaohua; Chen, Yiping

doi:10.1002/dvdy.22748

Cited by 42 publications

(59 citation statements)

References 36 publications

(66 reference statements)

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“…However, whether or not loss of Noggin alters the development of Meckel’s cartilage has not been reported. In our and other’s previous studies on the effects of overdosed BMP activity on the development of palate, tooth, and temporomandibular joint using Noggin mutant mice as a model, the formation of significantly enlarged Meckel’s cartilage was observed (He et al, 2010; Lana-Elola et al, 2011; Wang et al, 2011; Hu et al, 2012). In the present study, we followed up our previous observation by detailed analysis of the phenotype in Noggin mutants with focus on the middle portion of Meckel’s cartilage.…”

Section: Introductionmentioning

confidence: 60%

Enhanced BMP signaling prevents degeneration and leads to endochondral ossification of Meckel′s cartilage in mice

Wang

Zheng

Chen

et al. 2013

Developmental Biology

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Meckel’s cartilage is a transient supporting tissue of the embryonic mandible in mammals, and disappears by taking different ultimate cell fate along the distal-proximal axis, with the majority (middle portion) undergoing degeneration and chondroclastic resorption. While a number of factors have been implicated in the degeneration and resorption processes, signaling pathways that trigger this degradation are currently unknown. BMP signaling has been implicated in almost every step of chondrogenesis. In this study, we used Noggin mutant mice as a model for gain-of-BMP signaling function to investigate the function of BMP signaling in Meckel’s cartilage development, with a focus on the middle portion. We showed that Bmp2 and Bmp7 are expressed in early developing Meckels’ cartilage, but their expression disappears thereafter. In contrast, Noggin is expressed constantly in Meckel’s cartilage throughout the entire gestation period. In the absence of Noggin, Meckel’s cartilage is significantly thickened attributing to dramatically elevated cell proliferation rate associated with enhanced phosphorylated Smad1/5/8 expression. Interestingly, instead of taking a degeneration fate, the middle portion of Meckel’s cartilage in Noggin mutants undergoes chondrogenic differentiation and endochondral ossification contributing to the forming mandible. Chondrocyte-specific expression of a constitutively active form of BMPRIa but not BMPRIa leads enlargement of Meckel’s cartilage, phenocopying the consequence of Noggin deficiency. Our results demonstrate that elevated BMP signaling prevents degeneration and leads to endochondral ossification of Meckel’s cartilage, and support the idea that withdrawal of BMP signaling is required for normal Meckel’s cartilage development and ultimate cell fate.

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Section: Introductionmentioning

confidence: 60%

Enhanced BMP signaling prevents degeneration and leads to endochondral ossification of Meckel′s cartilage in mice

Wang

Zheng

Chen

et al. 2013

Developmental Biology

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“…Whereas the blastemal formation of these two major components of the TMJ occurs independently, the presence of the condyle is required for the sustained development of the glenoid fossa (Wang et al 2011; Gu et al 2014). However, the TMJ condyle and disc can develop in the absence of the glenoid fossa (Purcell et al 2012).…”

Section: Discussionmentioning

confidence: 99%

“…However, the TMJ condyle and disc can develop in the absence of the glenoid fossa (Purcell et al 2012). Although previous studies of TMJ development have been largely focused on the condyle and the articular disc, developmental defects in the glenoid fossa have been reported only in a few genetically modified mouse models (Wang et al 2011; Purcell et al 2012; Gu et al 2014). In these mouse models, with an absent or dislocated condyle, inactivation of Spry1 and Spry2 , or elevated BMPR-1A mediated signaling, the primordia of the glenoid fossa form nevertheless but became degenerated.…”

Section: Discussionmentioning

confidence: 99%

“…Conditional Ihh transgenic mice ( pMes-Ihh ) were generated by pronuclear injection of the pMes-Ires-Egfp vector containing the full-length cDNA of mouse Ihh , as described previously (Xiong et al 2009; He et al 2010). The pMes-Ihh transgenic vector was constructed by inserting the Ihh sequence into the site downstream of a LoxP -flanked STOP cassette under the control of the β-actin promoter and upstream of the Ires-Egfp sequences.…”

Section: Methodsmentioning

confidence: 99%

“…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%

See 2 more Smart Citations

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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Temporomandibular Joint Development

2013

Stem Cells in Craniofacial Development and Regeneration

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Tissue interaction is required for glenoid fossa development during temporomandibular joint formation

Cited by 42 publications

References 36 publications

Enhanced BMP signaling prevents degeneration and leads to endochondral ossification of Meckel′s cartilage in mice

Enhanced BMP signaling prevents degeneration and leads to endochondral ossification of Meckel′s cartilage in mice

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

Temporomandibular Joint Development

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