Knockdown of long non‑coding RNA AK094629 attenuates the interleukin‑1β induced expression of interleukin‑6 in synovium‑derived mesenchymal stem cells from the temporomandibular joint

• DOI: 10.3892/mmr.2020.11193
• Publication Date: 2020-05-27T22:11:57Z
• Authors: Jiaxin Jia; Jiadong Sun; Wenting Liao; Lingling Qin; Kai Su; Yiqing He; Jiaqiang Zhang; Ronchung Yang; Zhiguang Zhang; Yangpeng Sun
• Keywords: Transcriptional Activation; 0303 health sciences; Temporomandibular Joint; Interleukin-6; Interleukin-1beta; Synovial Membrane; Mesenchymal Stem Cells; Articles; Temporomandibular Joint Disorders; MAP Kinase Kinase Kinase 4; p38 Mitogen-Activated Protein Kinases; Up-Regulation; 03 medical and health sciences; Gene Knockdown Techniques; Osteoarthritis; Humans; RNA, Long Noncoding; Cells, Cultured

Interleukin (IL)‑1β is a key promotor in the pathogenesis of temporomandibular joint osteoarthritis. Differentiation stem cells to cartilage crucial repair mechanism articular damage, and IL‑1β has been reported impede differentiation by upregulating secretion IL‑6, an important inflammatory factor. Long non‑coding RNAs (lncRNAs) regulate number physiological pathological processes, but whether lncRNA AK094629 contributes mediated induction inflammation remains unclear. Therefore, aim present study was investigate effect on IL‑1β‑induced IL‑6 expression synovial‑derived mesenchymal (SMSCs) joints. The results demonstrated that synovial tissue patients with osteoarthritis positively correlated IL‑1β. In addition, upregulated SMSCs vitro, knockdown inhibited upregulation IL‑6. also downregulated mitogen‑activated protein kinase 4 (MAP3K4), which IL‑1β, whereas MAP3K4 did not affect AK094629, reversed SMSCs. conclusion, attenuated IL‑1β‑regulated inhibiting MAP3K4. may be potential novel therapeutic target for treatment