MicroRNA-23a inhibits osteogenic differentiation of human bone marrow-derived mesenchymal stem cells by targeting LRP5. (March 2016)

• Record Type: Journal Article
• Authors: Li, Tao; Li, Hongling; Wang, Yingzhen; Li, Tangping; Fan, Junfen; Xiao, Ke; Zhao, Robert Chunhua; Weng, Xisheng
• Is Part Of: International journal of biochemistry & cell biology. Volume 72(2016:Mar.)
• Page Start: 55
• Page End: 62
• Publication Date: 2016-03
• Subjects: microRNA-23a -- Human bone marrow-derived mesenchymal stem cells -- Osteogenic differentiation -- LRP5; Biochemistry -- Periodicals; Cytology -- Periodicals; Biochemistry -- Periodicals; Cell Biology -- Periodicals; Biochimie -- Périodiques; Cytologie -- Périodiques; Biochimie; Cytologie; Biochemistry; Cytology; Ressource Internet (Descripteur de forme); Périodique électronique (Descripteur de forme); Periodicals; 572.05
• DOI: 10.1016/j.biocel.2016.01.004
• Languages: English
• ISSNs: 1357-2725

Abstract

Abstract: Emerging evidence indicates that microRNAs (miRNA, or miR) play vital roles in regulating osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs). Elucidation of the molecular mechanisms that govern BMSCs osteogenic differentiation is of paramount importance for improving the treatment of bone-related diseases. In our current study, we investigated the role of miR-23a in BMSCs osteogenesis. Our results revealed that miR-23a was significantly downregulated during osteogenic differentiation. Overexpression of miR-23a inhibited osteogenic differentiation of hBMSCs in vitro, whereas downregulation of miR-23a enhanced the process. Target prediction analysis and dual luciferase reporter assays confirmed that low-density lipoprotein (LDL)-receptor-related protein 5 (LRP5) was a direct target of miR-23a. Furthermore, knockdown of LRP5 inhibited osteogenic differentiation of hBMSCs, similar to the effect observed in upregulation miR-23a. Our data indicate that miR-23a plays an inhibitory role in osteogenic differentiation of hBMSCs, which may act by targeting LRP5.