Abstract
Increasing evidence has demonstrated that the dysregulated expression of long noncoding RNAs (lncRNAs) has important roles in the progression of osteoarthritis (OA), but the function of the lncRNA SNHG15 remains unclear. In the present study, we observed that SNHG15 was downregulated in OA cartilage tissues and IL-1β-induced chondrocytes. The lower expression of SNHG15 was negatively associated with the observed modified Mankin scale scores, extracellular matrix (ECM) degradation and chondrocyte apoptosis. Downregulated expression of SNHG15 increased chondrocyte viability and decreased chondrocyte apoptosis and ECM degradation in vitro and reduced damage to articular cartilage in vivo. Mechanistically, we demonstrated that SNHG15 overexpression promotes the expression of BCL2L13 by sponging miR-141-3p. The higher expression of miR-141-3p was negatively correlated with SNHG15 and BCL2L13 levels in OA cartilage tissues, and a positive correlation was also shown between SNHG15 and BCL2L13 levels. Furthermore, ectopic expression of miR-141-3p or knockdown of BCL2L13 expression could both reduce the effects of SNHG15 on chondrocyte proliferation, apoptosis and ECM degradation. Collectively, these findings reveal that SNHG15 inhibits OA progression by acting as an miR-141-3p sponge to promote BCL2L13 expression, suggesting that knockdown of SNHG15 expression in chondrocytes can be a potential therapeutic strategy to ameliorate OA progression.