A discoidin domain receptor 1 knock-out mouse as a novel model for osteoarthritis of the temporomandibular joint
2014 | journal article. A publication with affiliation to the University of Göttingen.
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A discoidin domain receptor 1 knock-out mouse as a novel model for osteoarthritis of the temporomandibular joint
Schminke, B.; Muhammad, H.; Bode, C.; Sadowski, B.; Gerter, R.; Gersdorff, N. & Buergers, R. et al. (2014)
Cellular and Molecular Life Sciences, 71(6) pp. 1081-1096. DOI: https://doi.org/10.1007/s00018-013-1436-8
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- Authors
- Schminke, Boris; Muhammad, Hayat; Bode, Christa; Sadowski, Boguslawa; Gerter, Regina; Gersdorff, Nikolaus; Buergers, Ralf; Monsonego-Ornan, Efrat; Rosen, Vicki; Miosge, Nicolai
- Abstract
- Discoidin domain receptor 1 (DDR-1)-deficient mice exhibited a high incidence of osteoarthritis (OA) in the temporomandibular joint (TMJ) as early as 9 weeks of age. They showed typical histological signs of OA, including surface fissures, loss of proteoglycans, chondrocyte cluster formation, collagen type I upregulation, and atypical collagen fibril arrangements. Chondrocytes isolated from the TMJs of DDR-1-deficient mice maintained their osteoarthritic characteristics when placed in culture. They expressed high levels of runx-2 and collagen type I, as well as low levels of sox-9 and aggrecan. The expression of DDR-2, a key factor in OA, was increased. DDR-1-deficient chondrocytes from the TMJ were positively influenced towards chondrogenesis by a three-dimensional matrix combined with a runx-2 knockdown or stimulation with extracellular matrix components, such as nidogen-2. Therefore, the DDR-1 knock-out mouse can serve as a novel model for temporomandibular disorders, such as OA of the TMJ, and will help to develop new treatment options, particularly those involving tissue regeneration.
- Issue Date
- 2014
- Status
- published
- Publisher
- Springer
- Journal
- Cellular and Molecular Life Sciences
- ISSN
- 1420-9071; 1420-682X