Open AccessmiR-106a mimics the nuclear factor-κB signalling pathway by targeting DR6 in rats with osteoarthritis
Author(s) -
Liangyu Cui,
Yu Han,
Zhijie Dong
Publication year - 2020
Publication title -
archives of medical science/archives of medical science (online)
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 46
eISSN - 1896-9151
pISSN - 1734-1922
DOI - 10.5114/aoms.2020.92831
Subject(s) - inflammation , cartilage , in vivo , osteoarthritis , apoptosis , lipopolysaccharide , cytokine , nf κb , medicine , chondrocyte , in vitro , cancer research , signal transduction , chemistry , microbiology and biotechnology , immunology , pathology , biology , biochemistry , anatomy , alternative medicine
Introduction Osteoarthritis (OA) is a common inflammatory joint disease characterised by progressive cartilage destruction. Management of this condition remains a significant challenge, and new therapies are required. We investigated the protective effects of miR-106a mimics in a murine model of OA. Material and methods This study was performed using both in vitro and in vivo OA models. Primary chondrocytes were isolated from female rats, with inflammation induced via treatment with lipopolysaccharide (LPS). Then the effects of a miR-106a mimic were examined based on the level of inflammatory cytokine production and apoptotic signalling following LPS stimulation. An in vivo rat model of OA was generated by injecting LPS into the anterior cruciate ligament, followed by treatment with miR-106a mimics. Then, inflammatory and apoptotic protein expression was assessed in the cartilage tissue. Results Treatment with miR-106a mimic reduced the levels of inflammatory cytokines and apoptotic proteins in cartilage tissues following LPS-induced inflammation. Furthermore, the mimic ameliorated the expression of DR-6 mRNA and DR6, IB, and p65 proteins in chondrocytes. Similar effects were seen in the in vivo model, with the mimic attenuating expression of NF-B, p65, IB, and DR6 proteins and improving histopathological outcomes in the chondrocytes of OA rats. Conclusions Treatment with miR-106a mimic ameliorates inflammation in cartilage tissues of OA subjects by activating death receptor 6 via the NF-B signalling pathway.