Expression data of wild type and DDR-1-KO mice TMJ-cartilage

The discoidin domain receptor 1 (DDR-1) deficient mice exhibit a high incidence of osteoarthritis (OA) in the temporomandibular joint (TMJ) already at early age. Young DDR-1 knock-out mice show typical histological signs of OA, like, surface fissures, loss of proteoglycans, cluster formation of the chondrocytes, altered collagen types as well as atypical arrangement of the collagen fibrils. The isolated chondrocytes from the TMJ exhibit an osteoarthritic character with high amounts of Runt-related transcription factor 2 (runx-2) and collagen type I compared to low levels of SRY (sex determining region Y)-box 9 (sox-9) and aggrecan. Especially, the amount of discoidin domain receptor 2 (DDR2) is increased, which is key player of OA in this model. The gene expression as well as the proteins of the DDR-1-deficient chondrocytes from the TMJ could be influenced by a three dimensional matrix, combined with a knockdown of runx-2 or the stimulation with components of the extracellular matrix, for example nidogen-2. These manipulations caused the osteoarthritic chondrocytes of DDR-1-deficient mice to change their gene expression towards a signature of more physiological cartilage and will open new possibilities for future regenerative treatment options of temporomandibular disorders like OA of the TMJ. We used microarrays to detect the differences in gene-expression of wild type and Discoidin Domain Receptor 1 Tyrosine Kinase (DDR-1)-KO mice TMJ-cartilage. RNA was extracted directly of the madibular condyle cartilage