Deletion of Axin1 in condylar chondrocytes leads to osteoarthritis ‐like phenotype in temporomandibular joint via activation of β‐catenin and FGF signaling

We have generated Axin1 conditional knockout (KO) mice by targeting aggrecan ‐expressing condylar cartilage cells in the temporomandibular joint (TMJ). The Axin1 conditional KO mice showed TMJ osteoarthritis (OA)‐like phenotype, probably through activation of β‐catenin and fibroblast growth factor (FGF) signaling. Osteoarthritis (OA) in the temporomandibular joint (TMJ) is a degenerative disease in the adult, which is characterized by the pathological degeneration of condylar cartilage. Axin1 plays a critical role in the regulation of cartilage development and homeostasis. To determine the role of Axin1 in TMJ tissue at the adult stage, we generatedAxin1Agc1ER mice, in whichAxin1 was deleted inaggrecan‐expressing chondrocytes at 2 months of age. Histology, histomorphometry, and immunostaining analyses were performed using TMJ tissues harvested from 4‐ and 6‐month‐old mice after tamoxifen administration. Total RNA isolated from TMJ cartilage of 6‐month‐old mice was used for gene expres sion analysis. Progressive OA‐like degeneration was observed in condylar cartilage inAxin1 knockout (KO) mice with loss of surface continuity and the formation of vertical fissures. In addition, reduced alcian blue staining in condylar cartilage was also found inAxin1 KO mice. Immunostaining and reverse transcription quantitative polymerase chain reaction (qRT ‐PCR) assays revealed disturbed homeostasis in condylar cartilage with increased expressions of MMP13 and Adamts5 ...
Source: Journal of Cellular Physiology - Category: Cytology Authors: Tags: ORIGINAL RESEARCH ARTICLE Source Type: research