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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >MicroRNA fingerprints during human megakaryocytopoiesis
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MicroRNA fingerprints during human megakaryocytopoiesis

机译：人类巨核细胞生成过程中的MicroRNA指纹

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摘要

microRNAs are a highly conserved class of noncoding RNAs with important regulatory functions in proliferation, apoptosis, development, and differentiation. To discover novel regulatory pathways during megakaryocytic differentiation, we performed microRNA expression profiling of in vitro-differentiated megakaryocytes derived from CD34(+) hematopoietic progenitors. The main finding was down-regulation of miR-10a, miR-126, miR-106, miR-10b, miR-17 and miR-20. Hypothetically, the down-regulation of microRNAs unblocks target genes involved in differentiation. We confirmed in vitro and in vivo that miR-130a targets the transcription factorMAFB, which is involved in the activation of the GPIIB promoter, a key protein for platelet physiology. In addition, we found that miR-10a expression in differentiated megakaryocytes is inverse to that of HOXA1, and we showed that HOXA1 is a direct target of miR-10a. Finally, we compared the microRNA expression of megakaryoblastic leukemic cell lines with that of in vitro differentiated megakaryocytes and CD34+ progenitors. This analysis revealed up-regulation of miR-101, miR-126, miR-99a, miR-135, and miR-20. Our data delineate the expression of microRNAs during megakaryocytopoiesis and suggest a regulatory role of microRNAs in this process by targeting megakaryocytic transcription factors.
机译：microRNA是一类高度保守的非编码RNA，在增殖，凋亡，发育和分化中具有重要的调控功能。为了发现巨核细胞分化过程中的新型调控途径，我们对源自CD34（+）造血祖细胞的体外分化巨核细胞进行了microRNA表达谱分析。主要发现是miR-10a，miR-126，miR-106，miR-10b，miR-17和miR-20的下调。假设地，microRNA的下调解除了与分化有关的靶基因的封闭。我们在体外和体内证实了miR-130a靶向转录因子MAFB，该转录因子参与了GPIIB启动子的激活，GPIIB启动子是血小板生理的关键蛋白。此外，我们发现在分化的巨核细胞中miR-10a表达与HOXA1相反，并且我们证明HOXA1是miR-10a的直接靶标。最后，我们比较了巨核细胞白血病细胞系与体外分化的巨核细胞和CD34 +祖细胞的microRNA表达。该分析揭示了miR-101，miR-126，miR-99a，miR-135和miR-20的上调。我们的数据描述了巨核细胞生成过程中microRNA的表达，并暗示了microRNA在此过程中通过靶向巨核细胞转录因子的调控作用。

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