Silencing lncRNA HOTAIR declines synovial inflammation and synoviocyte proliferation and promotes synoviocyte apoptosis in osteoarthritis rats by inhibiting Wnt/β-catenin signaling pathway.

Osteoarthritis (OA) is a degenerative injury of the articular cartilage and reactive hyperplasia of the articular rim and subchondral bone. Due to its poor prognosis, this study is to research the influences of lncRNA HOTAIR on synovial inflammation and synoviocyte apoptosis and proliferation in OA rats by regulating the Wnt/β-catenin pathway. Rat OA model was constructed by means of cruciate ligament resection, and the successfully modeled rats were injected with sh-HOTAIR, or Wnt/β-catenin pathway activator (LiCl), and synoviocytes were transfected with sh-HOTAIR or LiCl for investigation of the influences of HOTAIR and Wnt/β-catenin pathway on synoviocytes proliferation and apoptosis. ELISA and RT-qPCR were used to detect the levels of IL-1β, IL-6 and TNF-α in serum, synovial tissue and synoviocytes in rats, respectively. The protein levels of bax, bcl-2, wnt1 and β-catenin in synovial tissue and synoviocytes were tested by Western blot analysis. Highly expressed HOTAIR existed in synovial tissue and synoviocytes of rats. There were declining arthritis index, inflammation, synoviocytes proliferation, cycle progression and promoted synoviocytes apoptosis by silencing HOTAIR and inhibited Wnt/β-catenin pathway. Down-regulation of HOTAIR could reverse the effect of LiCl on progression of OA rats. There was strained activation of Wnt/β-catenin pathway via declining HOTAIR. This study suggests that silencing lncRNA HOTAIR and inhibited Wnt/β-catenin pathway decline synovial inflammation and synoviocyte proliferation and promote apoptosis in OA rats.