Cartilage generation and degradation are controlled by miRNAs. Our previous study showed miR-23a-3p was downregulated during chondrogenic differentiation in chondrogenic human adipose-derived mesenchymal stem cells (hADSCs). In the present study, we explored the function of miR-23a-3p in chondrogenesis differentiation. The role of miR-23a-3p in chondrogenic differentiation potential of hADSCs was assessed by Alcian blue staining, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot. We show that miR-23a-3p suppressed the chondrogenic differentiation of hADSCs. LncRNA SNHG5 interacted with miR-23a-3p, and suppression or overexpression of SNHG5 correlates with inhibition and promotion of hADSC chondrogenic differentiation, respectively. We have determined that SNHG5 can sponge miR-23a-3p to regulate the expression of SOX6/SOX5, transcription factors that play essential roles in chondrocyte differentiation. Furthermore, the overexpression of SNHG5 activates the JNK/MAPK/ERK pathway. In conclusion, miR-23a-3p regulated by lncRNA SNHG5 suppresses the chondrogenic differentiation of human adipose-derived stem cells via targeting SOX6/SOX5.

中文翻译：

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LncRNA SNHG5调控的miR-23a-3p通过靶向SOX6/SOX5抑制人脂肪干细胞的软骨分化

软骨的生成和降解由 miRNA 控制。我们之前的研究表明 miR-23a-3p 在软骨形成的人脂肪源间充质干细胞 (hADSCs) 的软骨分化过程中被下调。在本研究中，我们探讨了 miR-23a-3p 在软骨形成分化中的功能。通过阿尔辛蓝染色、定量实时聚合酶链反应 (qRT-PCR) 和蛋白质印迹评估 miR-23a-3p 在 hADSCs 软骨形成分化潜能中的作用。我们表明 miR-23a-3p 抑制了 hADSCs 的软骨形成分化。LncRNA SNHG5 与 miR-23a-3p 相互作用，SNHG5 的抑制或过表达分别与 hADSC 软骨形成分化的抑制和促进相关。我们已经确定 SNHG5 可以吸收 miR-23a-3p 以调节 SOX6/SOX5 的表达，SOX6/SOX5 在软骨细胞分化中起重要作用的转录因子。此外，SNHG5 的过表达激活了 JNK/MAPK/ERK 通路。总之，受 lncRNA SNHG5 调控的 miR-23a-3p 通过靶向 SOX6/SOX5 抑制人脂肪干细胞的软骨分化。