miR-23a-3p regulated by LncRNA SNHG5 suppresses the chondrogenic differentiation of human adipose-derived stem cells via targeting SOX6/SOX5
miR-23a-3p regulated by LncRNA SNHG5 suppresses the chondrogenic differentiation of human adipose-derived stem cells via targeting SOX6/SOX5
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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
DOI：
10.1007/s00441-020-03289-4
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发表时间：
2020-09-22
影响因子：
3.6
通讯作者：
Tian, Xiaobin
中科院分区：
文献类型：
--
作者：
Yang, Zhen;Ren, Zhijing;Tian, Xiaobin
胡萝卜素的产生和降解受miRNA控制。我们先前的研究显示miR-23 a-3 p在软骨形成的人脂肪来源的间充质干细胞（hADSC）的软骨形成分化过程中下调。在本研究中，我们探讨了miR-23 a-3 p在软骨形成分化中的功能。通过阿辛蓝染色、实时定量聚合酶链反应（qRT-PCR）和Western blot评估miR-23 a-3 p在hADSC的软骨分化潜能中的作用。我们发现miR-23 a-3 p抑制hADSC的软骨分化。LncRNA SNHG 5与miR-23 a-3 p相互作用，SNHG 5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SNHG 5可以海绵miR-23 a-3 p来调节SOX 6/SOX 5的表达，SOX 6/SOX 5是在软骨细胞分化中起重要作用的转录因子。此外，SNHG 5的过表达激活JNK/MAPK/ERK通路。总之，由lncRNA SNHG 5调控的miR-23 a-3 p通过靶向SOX 6/SOX 5抑制人脂肪源性干细胞的软骨分化。
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.