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miR-23a/b regulates the balance between osteoblast and adipocyte differentiation in bone marrow mesenchymal stem cells

机译:miR-23a / b调节骨髓间充质干细胞中成骨细胞与脂肪细胞分化之间的平衡

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Age-related osteoporosis is associated with the reduced capacity of bone marrow mesenchymal stem cells (BMSCs) to differentiate into osteoblasts instead of adipocytes. However, the molecular mechanisms that decide the fate of BMSCs remain unclear. In our study, microRNA-23a, and microRNA-23b (miR-23a/b) were found to be markedly downregulated in BMSCs of aged mice and humans. The overexpression of miR-23a/b in BMSCs promoted osteogenic differentiation, whereas the inhibition of miR-23a/b increased adipogenic differentiation. Transmembrane protein 64 (Tmem64), which has expression levels inversely related to those of miR-23a/b in aged and young mice, was identified as a major target of miR-23a/b during BMSC differentiation. In conclusion, our study suggests that miR-23a/b has a critical role in the regulation of mesenchymal lineage differentiation through the suppression of Tmem64.
机译:与年龄有关的骨质疏松症与骨髓间充质干细胞(BMSCs)分化为成骨细胞而不是脂肪细胞的能力降低有关。但是,决定BMSC命运的分子机制仍不清楚。在我们的研究中,发现在老年小鼠和人类的BMSC中,microRNA-23a和microRNA-23b(miR-23a / b)明显下调。 BMSCs中miR-23a / b的过表达促进成骨分化,而抑制miR-23a / b则增加成脂分化。跨膜蛋白64(Tmem64)在成年和年轻小鼠中的表达水平与miR-23a / b呈负相关,被确定为BMSC分化过程中miR-23a / b的主要靶标。总之,我们的研究表明miR-23a / b通过抑制Tmem64在调节间充质谱系分化中起关键作用。

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