Metabolisms of extracellular matrix in temporomandibular joint

透明质酸（HA）寡糖作为竞争性受体拮抗剂，从细胞表面置换HA并诱导细胞信号传导事件。我们确定了软骨细胞CD44.HA相互作用破坏后聚集蛋白聚糖酶的表达和功能的变化。破坏软骨细胞CD44.HA与HA寡糖的相互作用可诱导ADAMTS-4和ADAMTS-5的转录。HA寡糖还诱导关节软骨细胞中具有ADAMTS-4的锚定MT4-MMP。NF-κ B途径的抑制阻断了HA寡糖介导的聚集蛋白聚糖酶刺激。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诱导基质降解，并通过NF-κ B信号通路的激活提高聚集蛋白聚糖酶。

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.