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Overexpression of Dlx2 leads to postnatal condyle degradation.

Dai J, Si J, Zhu X, Zhang L, Wu D, Lu J, Ouyang N, Wang X, Shen G - Mol Med Rep (2016)

Bottom Line: The model was constructed and the phenotype observed using gross observation, micro‑CT scan and histological examination.The model determined that overexpression of Dlx2 may lead to postnatal condyle malformation, subchondral bone degradation and irregular histological structure of the condylar cartilage.In addition, the expression of osteocalcin in the condyle region was markedly downregulated, whereas expression of msh homeobox 2 was upregulated.

View Article: PubMed Central - PubMed

Affiliation: Department of Oral and Cranio‑Maxillofacial Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011, P.R. China.

ABSTRACT
Distal-less homeobox 2 (Dlx2), a member of the Dlx family of transcription factors, is important for the development of craniofacial tissues. Previous studies based on knock‑out mutant mice revealed that Dlx2 primarily disturbed the development of tissues from maxillary arch. The present study used a transgenic mouse model to specifically overexpress Dlx2 in neural crest cells in order to investigate the role of Dlx2 overexpression in post‑natal condyle in mice. The model was constructed and the phenotype observed using gross observation, micro‑CT scan and histological examination. The model determined that overexpression of Dlx2 may lead to postnatal condyle malformation, subchondral bone degradation and irregular histological structure of the condylar cartilage. In addition, the expression of osteocalcin in the condyle region was markedly downregulated, whereas expression of msh homeobox 2 was upregulated. The results of the present study suggest that Dlx2 overexpression in cranial neural crest cells would disrupt the development of post‑natal condyle, which demonstrates that the expression level and the spatiotemporal expression patterns of Dlx2 may be important in regulating the development of post-natal condyle in mice, and also offered a possible temporal‑mandibular joint osteoarthritis model animal for future studies.

No MeSH data available.


Related in: MedlinePlus

Schematic representation of the Cre-mediated excision of the LacZ-Neo-STOP cassette in Wnt1Cre::iZEG-Dlx2 mice when iZEG-Dlx2 mice were mated with Wnt1-Cre mice.
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f1-mmr-14-02-1624: Schematic representation of the Cre-mediated excision of the LacZ-Neo-STOP cassette in Wnt1Cre::iZEG-Dlx2 mice when iZEG-Dlx2 mice were mated with Wnt1-Cre mice.

Mentions: Dlx2 C57BL/6J genetic background conditional overexpression transgenic mice (iZEG-Dlx2) were bred in Department of Oral and Cranio-Maxillofacial Surgery, Shanghai Ninth People's Hospital (Shanghai, China), and Wnt1-Cre transgenic mice were obtained from the Jackson Laboratory (Bar Harbor, Maine, USA). iZEG-Dlx2 transgenic mice were further bred with Wnt1-Cre transgenic mice to obtain the mice, which specifically overexpress Dlx2 in NCC derived tissues (Wnt1Cre::iZEG-Dlx2), as previously described (Fig. 1) (11). All animal experimental procedures were performed in compliance with the guidelines of the National Institute of Health in the United States and Institutional Animal Care and Use Committees of the Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, and were reviewed and approved by the Ethical Committees of the Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China (approval no, 2013-7).


Overexpression of Dlx2 leads to postnatal condyle degradation.

Dai J, Si J, Zhu X, Zhang L, Wu D, Lu J, Ouyang N, Wang X, Shen G - Mol Med Rep (2016)

Schematic representation of the Cre-mediated excision of the LacZ-Neo-STOP cassette in Wnt1Cre::iZEG-Dlx2 mice when iZEG-Dlx2 mice were mated with Wnt1-Cre mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4940110&req=5

f1-mmr-14-02-1624: Schematic representation of the Cre-mediated excision of the LacZ-Neo-STOP cassette in Wnt1Cre::iZEG-Dlx2 mice when iZEG-Dlx2 mice were mated with Wnt1-Cre mice.
Mentions: Dlx2 C57BL/6J genetic background conditional overexpression transgenic mice (iZEG-Dlx2) were bred in Department of Oral and Cranio-Maxillofacial Surgery, Shanghai Ninth People's Hospital (Shanghai, China), and Wnt1-Cre transgenic mice were obtained from the Jackson Laboratory (Bar Harbor, Maine, USA). iZEG-Dlx2 transgenic mice were further bred with Wnt1-Cre transgenic mice to obtain the mice, which specifically overexpress Dlx2 in NCC derived tissues (Wnt1Cre::iZEG-Dlx2), as previously described (Fig. 1) (11). All animal experimental procedures were performed in compliance with the guidelines of the National Institute of Health in the United States and Institutional Animal Care and Use Committees of the Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, and were reviewed and approved by the Ethical Committees of the Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China (approval no, 2013-7).

Bottom Line: The model was constructed and the phenotype observed using gross observation, micro‑CT scan and histological examination.The model determined that overexpression of Dlx2 may lead to postnatal condyle malformation, subchondral bone degradation and irregular histological structure of the condylar cartilage.In addition, the expression of osteocalcin in the condyle region was markedly downregulated, whereas expression of msh homeobox 2 was upregulated.

View Article: PubMed Central - PubMed

Affiliation: Department of Oral and Cranio‑Maxillofacial Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011, P.R. China.

ABSTRACT
Distal-less homeobox 2 (Dlx2), a member of the Dlx family of transcription factors, is important for the development of craniofacial tissues. Previous studies based on knock‑out mutant mice revealed that Dlx2 primarily disturbed the development of tissues from maxillary arch. The present study used a transgenic mouse model to specifically overexpress Dlx2 in neural crest cells in order to investigate the role of Dlx2 overexpression in post‑natal condyle in mice. The model was constructed and the phenotype observed using gross observation, micro‑CT scan and histological examination. The model determined that overexpression of Dlx2 may lead to postnatal condyle malformation, subchondral bone degradation and irregular histological structure of the condylar cartilage. In addition, the expression of osteocalcin in the condyle region was markedly downregulated, whereas expression of msh homeobox 2 was upregulated. The results of the present study suggest that Dlx2 overexpression in cranial neural crest cells would disrupt the development of post‑natal condyle, which demonstrates that the expression level and the spatiotemporal expression patterns of Dlx2 may be important in regulating the development of post-natal condyle in mice, and also offered a possible temporal‑mandibular joint osteoarthritis model animal for future studies.

No MeSH data available.


Related in: MedlinePlus