Metabolisms of extracellular matrix in temporomandibular joint

透明质酸(HA)寡糖作为竞争性受体拮抗剂，取代细胞表面的透明质酸，诱导细胞信号转导。我们测定了软骨细胞CD44-HA相互作用中断后聚集性聚糖酶表达和功能的变化。破坏软骨细胞CD44。HA与HA寡糖相互作用可诱导ADAMTS-4和ADAMTS-5的转录。HA寡糖也能诱导关节软骨细胞中的MT4-MMPs与ADAMTS-4结合。抑制核因子-kappaB通路可阻断HA寡糖介导的聚集聚糖酶的刺激。这些结果表明软骨细胞的破坏性变化。HA寡糖与基质的相互作用通过激活核因子-kappa B信号通路诱导基质降解和提升聚集聚糖酶。

Hyaluronan(HA) oligosaccharides serve as competitive receptor antagonists to displace HA from the cell surface and induce cell signaling events. We determined changes in the expression and function of aggrecanases after disruption of chondrocyte CD44.HA interactions. Disruption of chondrocyte CD44.HA interactions with HA oligosaccharides induced the transcription of ADAMTS-4 and ADAMTS-5.The association of GPI. anchored MT4-MMP with ADAMTS-4 was also induced in articular chondrocytes by HA oligosaccharides. Inhibition of the NF-kappa B pathway blocked HA oligosaccharides-mediated stimulation of aggrecanases. These results suggest that disruptive changes in chondrocyte. matrix interactions by HA oligosaccharides induce matrix degradation and elevate aggrecanases via the activation of the NF-kappa B signaling pathway.