The relevance between abnormal microRNA expression and osteoarthritis (OA) has been elaborated in recent studies. Hence, the present study aimed to assess the impact of miR-142-5p on chondrocyte growth and apoptosis.
To mimic OA-like chondrocyte damage, interleukin (IL)-1β was used for chondrocyte treatment. The expression of miR-142-5p, SGTB, long non-coding RNA (lncRNA) X inactive specific transcript (XIST) and involved molecules such as Col2A1, Bcl-2, MMP13 and Bax was determined via a quantitative reverse transcriptase-polymerase chain reaction and western blot analyses. Functional roles of miR-142-5p, SGTB and XIST were monitored in 5-ethynyl-2'-deoxyuridine, CCK-8 and TUNEL experiments. Rescue analyses were conducted to consolidate the effect of the XIST/miR-142-5p/SGTB axis on chondrocytes in OA.
miR-142-5p was down-regulated in IL-1β-treated chondrocytes, whereas SGTB and XIST levels were increased. Overexpression of miR-142-5p stimulated proliferation and retarded apoptosis in IL-1β-treated chondrocytes. Meanwhile, miR-142-5p elevation was correlated with an elevation of Col2A1 and Bcl-2, as well as a decline of MMP13 and Bax. A mechanistic study showed that miR-142-5p negatively regulated SGTB expression. Moreover, we found that lncRNA XIST could relieve the inhibition of miR-142-5p on SGTB expression. Augmentation of SGTB or suppression of miR-142-5p reversed the influence of XIST depletion on chondrocyte growth and apoptosis.
The present study has explored the fundamental role of miR-142-5p in IL-1β-treated chondrocytes, as well as the novel molecular mechanism constituted by miR-142-5p/SGTB/XIST in OA. Potentially, the results obtained may add new insight into OA pathogenesis.