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miR‐142‐5p protects against osteoarthritis through competing with lncRNA XIST
Author(s) -
Sun Pengfei,
Wu Yunpeng,
Li Xuezhou,
Jia Yuhua
Publication year - 2020
Publication title -
the journal of gene medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.689
H-Index - 91
eISSN - 1521-2254
pISSN - 1099-498X
DOI - 10.1002/jgm.3158
Subject(s) - xist , chondrocyte , long non coding rna , apoptosis , microrna , western blot , biology , tunel assay , messenger rna , microbiology and biotechnology , rna , cancer research , chemistry , cartilage , genetics , x inactivation , gene , anatomy , x chromosome
Background 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. Methods 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. Results 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. Conclusions 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.