MicroRNAs miR-96, miR-124, and miR-199a regulate gene expression in human bone marrow-derived mesenchymal stem cells
MicroRNAs miR-96, miR-124, and miR-199a regulate gene expression in human bone marrow-derived mesenchymal stem cells
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DOI：
10.1002/jcb.24144
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发表时间：
2012-08-01
影响因子：
4
通讯作者：
Laitala-Leinonen, Tiina K.
中科院分区：
文献类型：
--
作者：
Laine, Salla K.;Alm, Jessica J.;Laitala-Leinonen, Tiina K.
microrna是一种小的非编码rna，通过结合其靶mrna的3'-非翻译区（3'-UTR）在转录后水平上控制基因表达。他们提出了一种很有前途的工具来描述调节人间充质间质细胞（hMSCs）分化的分子机制，并改善hMSCs在治疗应用中的受控分化。本研究表明，在人骨髓源性MSCs的成骨、成脂和成软骨诱导过程中，miR-96、miR-124和miR-199a这三种microrna存在差异表达。miR-96的表达在成骨和脂肪形成过程中增加，但在软骨形成过程中没有增加。miR-124仅在脂肪细胞中表达，而miR-199a在成骨细胞和软骨细胞中表达上调。此外，对合成miRNA前体和抑制剂的功能研究表明，miR-96、miR-124和miR-199a调节了对hMSC分化重要基因的表达，如聚集蛋白、转录因子SOX9和脂肪酸结合蛋白4 （FABP4）。因此，调节miR-96、miR-124和miR-199a的表达可能有助于hMSC分化的特异性靶向，例如，基于msc的治疗。j .细胞。中国生物医学工程学报，2012,31(2):387 - 391。(c) 2012 Wiley期刊有限公司
MicroRNAs are small non-coding RNAs that control gene expression at the post-transcriptional level by binding to 3'-untranslated regions (3'-UTR) of their target mRNAs. They present a promising tool to delineate the molecular mechanisms regulating differentiation of human mesenchymal stromal cells (hMSCs) and to improve the controlled differentiation of hMSCs in therapeutic applications. Here we show that three microRNAs, miR-96, miR-124, and miR-199a, were differentially expressed during osteogenic, adipogenic, and chondrogenic induction of human bone marrow-derived MSCs. miR-96 expression was increased during osteogenesis and adipogenesis, but not during chondrogenesis. miR-124 was exclusively expressed in adipocytes, whereas miR-199a was upregulated in osteoblasts and chondrocytes. Furthermore, functional studies with synthetic miRNA precursors and inhibitors demonstrated that miR-96, miR-124, and miR-199a regulated the expression of genes important for hMSC differentiation, such as aggrecan, transcription factor SOX9, and fatty acid binding protein 4 (FABP4). Modulation of miR-96, miR-124, and miR-199a expression may thus be useful in specific targeting of hMSC differentiation, for e.g., MSC-based therapies. J. Cell. Biochem. 113: 26872695, 2012. (c) 2012 Wiley Periodicals, Inc.