MicroRNAs are involved in erythroid differentiation control
MicroRNAs are involved in erythroid differentiation control
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DOI：
10.1002/jcb.22156
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发表时间：
2009-06
影响因子：
4
通讯作者：
Gui-hua Yang;F. Wang;Jia Yu;Xiaoshuang Wang;Jinyun Yuan;Junwu Zhang
中科院分区：
文献类型：
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作者：
Gui-hua Yang;F. Wang;Jia Yu;Xiaoshuang Wang;Jinyun Yuan;Junwu Zhang
MicroRNA (miRNA) 是一类 17-25 个核苷酸的非编码 RNA 分子，通过翻译抑制或 mRNA 降解来调节基因表达。我们使用 miRNA 阵列来表征 K562 细胞在氯化血红素处理前后的 miRNA 变化。通过 Northern blot 分析验证了 5 种 miRNA 的差异表达。其中，在氯化血红素诱导后，miR-126表现出上调，而miR-103、miR-130a、miR-210和miR-18b表现出下调。对源自人脐带血的 CD34+ 细胞进行红系诱导后，观察到 5 种 miRNA 的相同表达趋势。选择 miR-103 并检查其在红系分化中的作用。 K562 中 miR-103 的过表达可以抑制氯高铁血红素诱导的 K562 红系分化，这表明该 miRNA 可能参与红细胞生成。我们证实 miR-103 靶向叉头盒 J2 (FOXJ2) 的 mRNA，叉头盒 J2 是一种参与许多组织发育的转录因子。我们的结果描绘了红细胞分化过程中 miRNA 的表达，并表明 miRNA 通过靶向与红细胞生成相关的 mRNA 在此过程中发挥调节作用。 J.细胞。生物化学。 107: 548–556, 2009。© 2009 Wiley-Liss, Inc.
MicroRNAs (miRNAs) are a class of 17–25 nucleotides non‐coding RNA molecules that regulate gene expression by either translational inhibition or mRNAs degradation. We used miRNA array to characterize miRNA variation of K562 cells before and after hemin treatment. The differential expression of five miRNAs was validated by Northern blot analysis. Among them, miR‐126 exhibited up‐regulation while miR‐103, miR‐130a, miR‐210, and miR‐18b exhibited down‐regulation after hemin induction. The same expression tendency of the five miRNAs was observed following erythroid induction of CD34+ cells derived from human cord blood. miR‐103 was selected and examined for its role in erythroid differentiation. Over‐expression of miR‐103 in K562 could inhibit hemin‐induced K562 erythroid differentiation, which suggests this miRNA may take part in erythropoiesis. We confirmed that miR‐103 targeting mRNA of forkhead box J2 (FOXJ2), a transcription factor that was involved in the development of many tissues. Our results delineated the expression of miRNAs during erythroid differentiation and suggested regulatory roles of miRNAs in this process by targeting mRNAs related to erythropoiesis. J. Cell. Biochem. 107: 548–556, 2009. © 2009 Wiley‐Liss, Inc.