A discoidin domain receptor 1 knock-out mouse as a novel model for osteoarthritis of the temporomandibular joint

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• 作者：Boris Schminke (1)
  Hayat Muhammad (1)
  Christa Bode (1)
  Boguslawa Sadowski (1)
  Regina Gerter (1)
  Nikolaus Gersdorff (1)
  Ralf Bürgers (1)
  Efrat Monsonego-Ornan (2)
  Vicki Rosen (3)
  Nicolai Miosge (1)
  
• 关键词：Temporomandibular joint ; Osteoarthritis ; Extracellular matrix ; Collagen receptor ; Chondrocyte signaling
• 刊名：Cellular and Molecular Life Sciences (CMLS)
• 出版年：2014
• 出版时间：March 2014
• 年：2014
• 卷：71
• 期：6
• 页码：1081-1096
• 全文大小：1,951 KB
• 作者单位：Boris Schminke (1)
  Hayat Muhammad (1)
  Christa Bode (1)
  Boguslawa Sadowski (1)
  Regina Gerter (1)
  Nikolaus Gersdorff (1)
  Ralf Bürgers (1)
  Efrat Monsonego-Ornan (2)
  Vicki Rosen (3)
  Nicolai Miosge (1)
  
  1. Oral Biology and Tissue Regeneration Work Group, Department of Prosthodontics, Medical Faculty, Georg-August-University, Robert Koch Stra?e 40, 37075, Goettingen, Germany
  2. Robert H. Smith Faculty of Agriculture, Food and Environment, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University of Jerusalem, P.O. Box 12, 76100, Rehovot, Israel
  3. Developmental Biology, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA, 02115, USA
  
• ISSN：1420-9071

文摘

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.