Differential regulation of proteoglycan 4 by IL-1alpha and TGF-beta1 in rat condylar chondrocytes

Objective: Proteoglycan 4 (PRG4) is a multifaceted cytoprotective glycoprotein that mediates the boundary lubrication of articular cartilages and maintains joint homeostasis and functions. However, the expression of PRG4 and associated regulatory mechanisms by growth factors and cytokines has not been fully clarified in the mandibular condylar cartilage. The purpose of this study was to investigate the effects of interleukin-1α (IL-1α) and transforming growth factor-β1 (TGF-β1) on the expression and secretion of PRG4 in the articular chondrocytes derived from rat mandibular condyle.

Methods: Articular chondrocytes were isolated from rat mandibular condyle and maintained in a monolayer culture system. After exposure to various concentrations of recombinant IL-1α and TGF-β1 alone or in combination, the PRG4 mRNA expression and protein accumulation in the cultured condylar chondrocytes were assessed by RT-PCR and ELISA, respectively.

Results: Exposure of chondrocytes to rhIL-1α resulted in a pronounced reduction in the expression and abundance of PRG4 in a time-dependent manner. In contrast, treatment with rhTGF-β1 significantly enhanced PRG4 synthesis and secretion in a dose-and time-dependent manner. Moreover, rhTGF-β1 was capable to antagonize the inhibitory effects on the PRG4 production induced by IL-1α pretreatment and reversed the PRG4 production in vitro.

Conclusions: Condylar cartilage production of PRG4 is highly regulated by growth factors and cytokines such as IL-1 and TGF-β1 that relevant to mandibular condyle repair and pathogenesis of temporomandibular joint (TMJ) osteoarthritis. These results suggested that enhanced biosynthesis and secretion of PRG4 may improve the TMJ function and become a potential therapeutic strategy for TMJ osteoarthritis.

Conflict of interest: None declared.

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Feb 5, 2018 | Posted by in Oral and Maxillofacial Surgery | Comments Off on Differential regulation of proteoglycan 4 by IL-1alpha and TGF-beta1 in rat condylar chondrocytes
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