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

Automated summary

Silencing of LINC00473 protects CHON-001 cells from IL-1 beta-induced cell injury by inhibiting the methylation of LMP-1 and interfering with the JNK/NF-kappa B signaling pathway. Therefore, LINC00473 may serve as a potential therapeutic target for osteoarthritis.