Long non-coding RNA H19 modulates proliferation and apoptosis in osteoarthritis via regulating miR-106a-5p.

Osteoarthritis (OA), a type of joint diseases, could result in breakdown of joint cartilage and underlying bone. Accumulating evidences suggested that long non-coding RNAs play important roles in OA progression. However, the underlying mechanism of H19 in OA is still not fully explored. The expression levels of H19 and miR-106a-5p in OA samples from patients or cultured chondrocytes were examined by quantitative real time polymerase chain reaction. Cell proliferation and apoptosis were analysed by MTT assay and flow cytometry, respectively. Western blotting was employed to detect the expression levels of PCNA, CyclinD1, Caspase 3 and Cleaved Caspase 3. StarBase database, luciferase assay and RNA immunoprecipitation were introduced to confirm the relationship between H19 and miR-106a-5p. The correlation of H19 and miR-106a-5p was analysed by Spearman rank analysis. H19 expression was upregulated, while miR-106a-5p level was downregulated in OA samples and IL-1b-treated chondrocytes. H19 overexpression inhibited the proliferation and induced apoptosis in IL-1b-treated chondrocytes, while H19 knockdown induced the opposite effect. Luciferase and RIP assay demonstrated that miR-106a-5p was a direct target of H19. miR-106a-5p overexpression led to proliferation promotion and apoptosis inhibition in chondrocytes treated by IL-1β and it reversed the effect of H19 addition. We conclude that H19 could regulate proliferation and apoptosis of chondrocytes treated by IL-1β in OA via sponging miR-106a-5p.