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    Prospective signs of cleidocranial dysplasia in Cebpb deficiency

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    Author
    Huang, B; Takahashi, K; Jennings, EA; Pumtang-on, P; Kiso, H; Togo, Y; Saito, K; Sugai, M; Akira, S; Shimizu, A; ...
    Date
    2014-05-13
    Source Title
    Journal of Biomedical Science
    Publisher
    BIOMED CENTRAL LTD
    University of Melbourne Author/s
    Jennings, Ernest
    Affiliation
    Anatomy and Neuroscience
    Metadata
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    Document Type
    Journal Article
    Citations
    Huang, B., Takahashi, K., Jennings, E. A., Pumtang-on, P., Kiso, H., Togo, Y., Saito, K., Sugai, M., Akira, S., Shimizu, A. & Bessho, K. (2014). Prospective signs of cleidocranial dysplasia in Cebpb deficiency. JOURNAL OF BIOMEDICAL SCIENCE, 21 (1), https://doi.org/10.1186/1423-0127-21-44.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/256257
    DOI
    10.1186/1423-0127-21-44
    Abstract
    BACKGROUND: Although runt-related transcription factor 2 (RUNX2) has been considered a determinant of cleidocranial dysplasia (CCD), some CCD patients were free of RUNX2 mutations. CCAAT/enhancer-binding protein beta (Cebpb) is a key factor of Runx2 expression and our previous study has reported two CCD signs including hyperdontia and elongated coronoid process of the mandible in Cebpb deficient mice. Following that, this work aimed to conduct a case-control study of thoracic, zygomatic and masticatory muscular morphology to propose an association between musculoskeletal phenotypes and deficiency of Cebpb, using a sample of Cebpb-/-, Cebpb+/- and Cebpb+/+ adult mice. Somatic skeletons and skulls of mice were inspected with soft x-rays and micro-computed tomography (μCT), respectively. Zygomatic inclination was assessed using methods of coordinate geometry and trigonometric function on anatomic landmarks identified with μCT. Masseter and temporal muscles were collected and weighed. Expression of Cebpb was examined with a reverse transcriptase polymerase chain reaction (RT-PCR) technique. RESULTS: Cebpb-/- mice displayed hypoplastic clavicles, a narrow thoracic cage, and a downward tilted zygomatic arch (p < 0.001). Although Cebpb+/- mice did not show the phenotypes above (p = 0.357), a larger mass percentage of temporal muscles over masseter muscles was seen in Cebpb+/- littermates (p = 0.012). The mRNA expression of Cebpb was detected in the clavicle, the zygoma, the temporal muscle and the masseter muscle, respectively. CONCLUSIONS: Prospective signs of CCD were identified in mice with Cebpb deficiency. These could provide an additional aetiological factor of CCD. Succeeding investigation into interactions among Cebpb, Runx2 and musculoskeletal development is indicated.

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