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取代HA并诱导细胞信号转导事件。我们测定了软骨细胞CD44破坏后聚集酶表达和功能的变化。HA交互。破坏软骨细胞CD44。HA与HA寡糖的相互作用诱导了ADAMTS-4和ADAMTS-5的转录。GPI协会。含ADAMTS-4的锚定MT4-MMP也被HA寡糖诱导到关节软骨细胞中。nf - κ B通路的抑制可阻断HA寡糖介导的聚合酶刺激。这些结果提示软骨细胞的破坏性改变。HA寡糖与基质的相互作用通过激活nf - κ B信号通路诱导基质降解并提高聚集酶。

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.