Deletion of Runx2 in condylar chondrocytes disrupts TMJ tissue homeostasis

@article{Liao2018DeletionOR,
  title={Deletion of Runx2 in condylar chondrocytes disrupts TMJ tissue homeostasis},
  author={Lifan Liao and Shanxing Zhang and Guang-qian Zhou and Ling Ye and Jian Huang and Lan Zhao and Di Chen},
  journal={Journal of Cellular Physiology},
  year={2018},
  volume={234},
  pages={3436 - 3444},
  url={https://api.semanticscholar.org/CorpusID:53241433}
}
It is demonstrated that Runx2 is required for chondrocyte proliferation and hypertrophy in TMJ cartilage and postnatal TMJCartilage growth and homeostasis, and that Run x2 may play an important role in regulation of chond rocyte‐derived subchondral bone remodeling.
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28 Citations
Background Citations
9
Methods Citations
1

28 Citations

Runx2 is required for postnatal intervertebral disc tissue growth and development

It is demonstrated that Runx2 may play an important role in postnatal disc tissue development through interacting with Ihh signaling.

Runx2 and Runx3 differentially regulate articular chondrocytes during surgically induced osteoarthritis development

It is shown that Runx3 protects adult articular cartilage by extracellular matrix protein production in normal conditions, while Runx2 exerts both catabolic and anabolic effects during inflammation.

Deletion of Bmal1 in aggrecan-expressing cells leads to mouse temporomandibular joint osteoarthritis.

It is demonstrated that Bmal1 was essential for TMJ tissue homeostasis and loss-of-function of Bmal1 in chondrocytes leads to the development of TMJ OA.

A PTHrP Gradient Drives Mandibular Condylar Chondrogenesis via Runx2

A Pthrp-mCherry knock-in reporter strain is used to map the localization of PTHrP+ cells in the MCC and define the function of PTHrP in the growing mandibular condyle, revealing a unique PTHrP gradient-directed mechanism that regulates MCC chondrogenesis.

Loss of miR‐204 and miR‐211 shifts osteochondral balance and causes temporomandibular joint osteoarthritis

Together, the results establish a key role of miR‐204/‐211 in maintaining the osteochondral homeostasis of the TMJ and counteracting OA pathogenesis through repressing the pro‐osteogenic factors including RUNX2 and β‐catenin.

Melatonin promotes the proliferation and differentiation of antler chondrocytes via RUNX2 dependent on the interaction between NOTCH1 and SHH signaling pathways.

Results showed that MT promoted the proliferation of antler chondrocytes and induced the differentiation of chondrocytes into hypertrophic chondrocytes as evidenced by the significant increase of collagen type X, alkaline phosphatase (ALP) and matrix metalloproteinase 13 (MMP13) expression and ALP activity, the well-established markers for hypertrophic chondrocytes.

Expression Profiling and Functional Analysis of Candidate Col10a1 Regulators Identified by the TRAP Program

32 candidate transcription factors recently identified by analyzing the 150-bp Col10a1 enhancer using the transcription factor affinity prediction (TRAP) program were analyzed and most of the differential expression pattern of these TFs conformed with the results obtained from ATDC5 cell model and primary mouse chondrocytes.

Fostamatinib alleviates temporomandibular joint osteoarthritis by maintaining cartilage homeostasis through MAPK/NF-κB and AKT/mTOR pathways.

Runx2 plays a central role in Osteoarthritis development

Transcriptomics analyses of IL-1β-stimulated rat chondrocytes in temporomandibular joint condyles and effect of platelet-rich plasma

31 References

Runx2-deficient mice lack mandibular condylar cartilage and have deformed Meckel’s cartilage

Findings indicate that Runx2 is essential for the formation of the mandibular condylar cartilage, as well as for normal development of Meckel’s cartilage and that muscle tissues influence mandible morphology.

Runx2 and Runx3 are essential for chondrocyte maturation, and Runx2 regulates limb growth through induction of Indian hedgehog.

Investigation of the involvement of Runx3 in chondrocyte differentiation by generating Runx2-and-Runx3-deficient (Runx2(-/-)3(-/-)) mice found that chondrospermia differentiation was inhibited depending on the dosages of Run x2 and Runx4, and Run x3- deficient mice showed a complete absence of chond rocyte maturation.

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This review summarizes and discusses the current knowledge and lack of knowledge about the chondrocyte differentiation pathway, from mesenchymal cells to growth plate and articular chONDrocytes, with a main focus on how it is controlled by tissue patterning and cell differentiation transcription factors.

Chondrocytes Directly Transform into Bone Cells in Mandibular Condyle Growth

A multipronged approach clearly demonstrates that a majority of chondrocytes in the fibrocartilaginous condylar cartilage, similar to hyaline cartilage in long bones, directly transform into bone cells during endochondral bone formation.

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Indian Hedgehog Roles in Post-natal TMJ Development and Organization

Analysis of the data shows, for the first time, that continuous Ihh action is required for completion of post-natal TMJ growth and organization and that lubricin overexpression in mutants may represent a compensatory response to sustain TMJ movement and function.

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The Runx (runt‐related protein) family of transcription factors plays important roles in different tissues and cell lineages and elucidation of the signaling pathways through Runx2 and Runx3 will unravel the complex mechanism of skeletal development.

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RUNX-2 contributes to the pathogenesis of OA through chondrocyte hypertrophy and matrix breakdown after the induction of joint instability, as compared with wild-type mice.

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It is suggested that Runx2 is absolutely required for endochondral ossification during embryonic and postnatal skeletogenesis, but that disrupting its expression in already committed osteoblasts as achieved here with the α1(I)‐collagen‐Cre driver does not affect overtly intramembranous and endochondrals Ossification.