Premium
miR‐382‐3p suppressed IL‐1β induced inflammatory response of chondrocytes via the TLR4/MyD88/NF‐κB signaling pathway by directly targeting CX43
Author(s) -
Lei Jinlai,
Fu Yahui,
Zhuang Yan,
Zhang Kun,
Lu Daigang
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28882
Subject(s) - chemistry , tlr4 , signal transduction , nf κb , matrix metalloproteinase , microbiology and biotechnology , nitric oxide synthase , interleukin , connexin , chondrocyte , inflammation , receptor , downregulation and upregulation , nitric oxide , medicine , cytokine , gap junction , biology , biochemistry , gene , in vitro , intracellular , organic chemistry
miR‐382‐3p has been reported to be upregulated in synovial membrane in knee osteoarthritis (OA). Nevertheless, its role in OA remains largely unknown. The aim of this study was to investigate the specific function and mechanisms of miR‐382‐3p in the course of OA. In this study, human OA chondrocytes were pretreated with interleukin‐1β (IL‐1β) at 5 ng/ml for 12 hr to stimulate inflammatory response and matrix metalloproteinases (MMPs) expression in chondrocytes. Meanwhile, miR‐382‐3p was downregulated in IL‐1β‐stimulated chondrocytes. In addition, we found that miR‐382‐3p directly interacts with connexin 43 (CX43) and attenuates the increase of cytochrome c oxidase polypeptide II, inducible nitric oxide synthase, and MMP‐1/13 that is induced by IL‐1β. Furthermore, our observations indicated that miR‐382‐3p inhibited the expression of Toll‐like receptor 4 (TLR4), Myeloid differentiation primary response 88 (MyD88) and nuclear factor κB (NF‐κB) in IL‐1β‐stimulated chondrocytes, while CX43 overexpression could partly reverse these decreases. In conclusion, miR‐382‐3p participated in OA may through the TLR4/MyD88/NF‐κB signaling pathway by directly targeting CX43.