Abstract

Osteoarthritis (OA) is a chronic joint disease and hard to cure at present. Alpha B-crystallin (CRYAB) has been identified as a downregulated gene in OA cartilage. However, the precise roles and underlying molecular mechanisms of CRYAB in OA progression have not been elucidated. In the present study, we found that the expression of CRYAB in cartilages from patients with OA was significantly lower than that in the cartilages from patients with no prior medical history of OA. We established mouse models with OA by destabilization of the medial meniscus (DMM) surgery and found that the expression of CRYAB in OA cartilage was lower than that in the normal cartilages, too. Moreover, we demonstrated that the expression of CRYAB was increased during chondrogenic differentiation and cartilage development. Functional assays revealed that overexpression of CRYAB promoted the proliferation of chondrocytes and inhibited apoptosis, while knockdown of CRYAB presented opposite results. In addition, overexpression of CRYAB upregulated the expression of anabolic markers, Col2a1 and ACAN, and reduced the expression of catabolic markers, MMP13 and ADAMTS5 . Conversely, knockdown of CRYAB blocked the expression of the anabolic markers and increased the expression of catabolic markers. Collectively, the results suggest that CRYAB promoted the proliferation and extracellular matrix production of chondrocytes, and inhibited chondrocytes apoptosis and cartilage degradation simultaneously. Thus, CRYAB might be a potential therapeutic target for OA treatment.