Abstract
Temporomandibular joint OA (TMJOA) is a common degenerative joint disease, leads to structural damage and ultimately loss of function. Matrix degradation is one of the first pathogenesis during the progression of OA, it was effective to inhibit matrix degradation to block the development of OA. In this study, an in vivo model (compressive mechanical force) and an in vitro model (IL-1β) were used to induce OA-like changes in TMJ cartilage and chondrocytes. We revealed lysyl oxidase like-2 (LOXL2) play a critical role in TMJOA. LOXL2 expression decreased in mechanical stress/IL-β induced TMJOA-like lesions in both in vivo models and in vitro models. Furthermore, recombinant LOXL2 (rhLOXL2) treatment ameliorated the degenerative changes induced by mechanical stress in vivo, including the thinning cartilage, down-expression of collagen II and proteoglycan, and over-expression of TNF-a, while LOXL2 antibody (anti-LOXL2) treatment exacerbated these changes. Mechanistically, the protection of LOXL2 in chondrocytes was induced partly through activation of the Integrin/FAK pathway. The inhibition of the Integrin/FAK pathway could neutralized the effects caused by rhLOXL2. Collectively, our study suggests that the LOXL2 plays a protective role in mechanical stress induced TMJOA-like changes, and the Integrin/FAK pathway may be a key downstream pathway in this process.
Highlights
Temporomandibular joint osteoarthritis (TMJ OA), the most common TMJ disease, is characterized by progressive degeneration of the articular c artilage[1,2,3]
lysyl oxidase like-2 (LOXL2) was downregulated in the TMJ OA cartilages induced by compressive mechanical force in vivo
To dissect the underlying function of LOXL2 proteins in the osteoarthritis chondrocytes induced by mechanical stress, we first manipulated a study to assess if LOXL2 expression correlate with the severity of osteoarthritis
Summary
Temporomandibular joint osteoarthritis (TMJ OA), the most common TMJ disease, is characterized by progressive degeneration of the articular c artilage[1,2,3]. Overload compressive mechanical stimulation has been proven to induce OA-like pathological changes in cartilage, including matrix degradation and the death of chondrocytes[4,5,6]. We hypothesized that LOXL2 protected cartilage by promoting the cross-linking of collagen to defense the degeneration of ECM in OA. To investigate this hypothesis, we detected the expression of LOXL2 in an established in vivo animal model of compressive mechanical force loading as r eported[4,6]. The study provides new insight into the role of LOXL2 in regulating cartilage thinning under mechanical stress and might facilitate the identification of new therapeutic targets for treating TMJ OA diseases
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