Knockdown of Long Non-coding RNA LINC00473 Protects CHON-001 Cells against Interleukin-1β-Induced Cell Injury

Osteoarthritis (OA) is a chronic joint disease with high prevalence. However, effective treatment options for OA are still lacking. It was previously reported that LINC00473 upregulated in patients and might be associated the progression of OA; however, role remains to investigated. CHON-001 human chondrocyte cells stimulated 10 ng/mL interleukin (IL)-1β were utilized mimic vitro. Protein expression, cell apoptosis proliferation investigated by Western blot, Annexin V propidium iodide (PI) double staining, counting-8 kit assay immunofluorescence staining respectively. The result indicated IL-1β triggered viability decrease cells, which alleviated knockdown. Meanwhile, IL-1β-induced upregulation cleaved caspase 3 Bax ameliorated Likewise, downregulation X-linked inhibitor protein In addition, knockdown protected against inhibiting methylation LIM mineralization (LMP)-1 gene. Moreover, c-Jun N-terminal kinase (JNK)/nuclear factor-kappaB (NF-κB) signaling pathway proved involved protective effect treated cells. Taken together, defended from induced injury via inhibition LMP-1. Thus, possibly act as novel therapeutic target OA.