DDX5 alleviates osteoarthritic temporomandibular joint by maintaining homeostasis of cartilage metabolism
Temporomandibular joint osteoarthritis (TMJOA) is a prevalent musculoskeletal disease without effective therapeutic measure. DDX5 regulated the progression of cancer,immune disease, as well as skin inflammation by activating a series of signal transduction pathways. However, the role of DDX5 in TMJOA has not been reported yet. The distribution of DDX5 in human cartilage was performed by HE, Safranin O and Masson staining. Moreover, the expression of DDX5 was unveiled by immunofluorescent analyses. The role of DDX5 in TMJOA was verified by UAC-induced TMJOA mice and Aggrecan-CreERT; DDX5flox/flox mice. The downstream protein expression profile of DDX5 were examined by RNA-Seq analysis. The DDX5 expression remarkably decreased in the condylar cartilage of patients with TMJOA. DDX5 decreased with cartilage degradation in UAC-Induced TMJOA mice. Cartilage specific DDX5 knockout induced cartilage degeneration. Mechanistically, the inhibition expression of DDX5 accelerates cartilage degeneration by activating NF-?B Signaling. Additionally, DDX5 overexpression alleviated the progression of TMJOA under excessive mechanical stress. Overall design: The downstream protein expression profile of DDX5 were examined by RNA-Seq analysis.