4.5 Article

Periostin Mediates Condylar Resorption via the NF-κB-ADAMTS5 Pathway

期刊

INFLAMMATION
卷 43, 期 2, 页码 455-465

出版社

SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-019-01129-4

关键词

temporomandibular disorders; signal transduction; cartilage; pressure; osteoarthritis

资金

  1. National Natural Science Foundation of China [81671010]
  2. Western Medicine Guidance Project of Shanghai Science and Technology Commission [16411960800]

向作者/读者索取更多资源

Although the up-regulation of periostin in osteoarthritic (OA) is found, its function on OA condyle caused by disc displacement is not clear. Our objective was to explore whether periostin has any effect on condylar resorption. We initially identified periostin-positive cells in temporomandibular joint osteoarthritic (TMJ-OA) cartilage. Furthermore, the vitro analysis confirmed that the expression of periostin in chondrocytes treated with a static pressure of 150 kpa and 200 kpa for 3 h by an in-house-designed pressure chamber. To explore the underlying mechanism, we found that periostin can induce I kappa B alpha phosphorylation and its subsequent degradation, leading to consequent p65 nuclear translocation and subsequent induction of ADAMTS5 expression, which is known to be detrimental to cartilage extracellular matrix production. Importantly, inhibiting NF-kappa B signaling, by BAY 11-7082 treatment, rescued periostin-induced ADAMTS5 up-regulation. This study elucidated the direct role of periostin in condylar resorption, which was found to occur via NF-kappa B-ADAMTS5 signaling. Inhibition of this pathway might provide a new strategy for TMJ-OA treatment.

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