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. 2020 Aug:52:101560.
doi: 10.1016/j.mcp.2020.101560. Epub 2020 Mar 21.

V体育平台登录 - LncRNA PVT1 induces chondrocyte apoptosis through upregulation of TNF-α in synoviocytes by sponging miR-211-3p

Kai Xu  1 , Zhen Meng  2 , Xin-Miao Xian  3 , Mo-Hong Deng  4 , Qing-Gong Meng  4 , Wei Fang  4 , Di Zhang  2 , Xing Long  5
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LncRNA PVT1 induces chondrocyte apoptosis through upregulation of TNF-α in synoviocytes by sponging miR-211-3p

Kai Xu et al. Mol Cell Probes. 2020 Aug.

Abstract

Temporomandibular joint osteoarthritis (TMJ OA) is an important subtype of temporomandibular disorders (TMD). Articular cartilage destruction is considered a common pathological feature of TMJ OA, which is reported to be mainly induced by chondrocyte apoptosis. Synovial sterile inflammation is an initial factor of TMJ OA-associated articular cartilage destruction. Therefore, determining the mechanism of synovial membrane inflammation-induced articular cartilage destruction in TMJ OA is important for the TMJ OA therapy. In this study, we detected the function of synoviocytes in chondrocyte apoptosis under lipopolysaccharide (LPS)-induced inflammatory conditions and explored the underlying mechanism. We found that synoviocytes in inflammatory conditions facilitated LPS-induced chondrocytes apoptosis by secreting increased Tumor Necrosis Factor α (TNF-α), which was induced by long non-coding RNA plasmacytoma variant translocation 1 (PVT1) upregulation VSports手机版. PVT1 served as a competing endogenous RNA that sponged the microRNA miR-211-3p and prevented the inhibition of TNF-α expression. In conclusion, our in vitro study revealed that PVT1 has a previously unknown role in chondrocyte apoptosis, which may also be a mechanism underlying synoviocyte involvement in TMJ OA. .

Keywords: Chondrocyte; Plasmacytoma variant translocation; Synoviocyte; TNF-α; Temporomandibular joint; miR-211-3p V体育安卓版. .

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Conflict of interest statement

Declaration of competing interest The authors declare that they have no competing interests.

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