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首页> 外文期刊>Journal of Cellular Physiology >MicroRNA-302a Stimulates Osteoblastic Differentiation by Repressing COUP-TFII Expression
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MicroRNA-302a Stimulates Osteoblastic Differentiation by Repressing COUP-TFII Expression

机译：微rna - 302 a刺激成骨细胞的分化的抑制COUP-TFII表达式

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Chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) is a potent transcription factor that represses osteoblast differentiation and bone formation. Previously, we observed that stimuli for osteoblast differentiation, such as bone morphogenetic protein 2 (BMP2), inhibits COUP-TFII expression. This study was undertaken to identify BMP2-regulated and COUP-TFII-targeting microRNAs (miRNAs), and to explore their regulatory roles in osteoblast differentiation. Based on in silico analysis, 12 miRNAs were selected and their expression in BMP2-treated MC3T3-E1 cells was examined. BMP2 induced miR-302a expression in dose- and time-dependent manners with the decrease in COUP-TFII expression. Runx2, a BMP2-downstream transcription factor, specifically regulated miR-302a expression and its promoter activity. A computer-based prediction algorithm led to the identification of two miR-302a binding sites on the 3'-untranslational region of COUP-TFII mRNA (S1: 620-626 bp, S2: 1,016-1,022 bp), and a luciferase assay showed that miR-302a directly targeted S1 and S2. Transfection of miR-302a precursor significantly enhanced expression of osteogenic marker genes with decreasing COUP-TFII mRNA and protein level, alkaline phosphatase activity and matrix mineralization. On the other hand, inhibition of miR-302a significantly attenuated BMP2-induced osteoblast specific gene expression, alkaline phosphatase activity, and matrix mineralization with increasing COUP-TFII mRNA and protein level. These results indicate that miR-302a is induced by osteogenic stimuli and promotes osteoblast differentiation by targeting COUP-TFII. MiR-302a could be a positive regulator for osteoblast differentiation. (C) 2014 Wiley Periodicals, Inc.
机译：鸡卵清蛋白上游启动子的转录因子II (COUP-TFII)是一种有效的转录因素压制成骨细胞分化和骨形成。刺激对成骨细胞分化,如骨形成蛋白2 (BMP2),抑制COUP-TFII表达式。识别BMP2-regulated和在成骨细胞中探索他们的监管角色分化。microrna选择和他们的表达BMP2-treated MC3T3-E1细胞检查。诱导mir - 302剂量和表达式时间与减少礼仪COUP-TFII表达式。转录因子,特别是监管mir - 302表达及其启动子活动。计算机预测算法导致的识别两个mir - 302上的结合位点3 ' -untranslational地区COUP-TFII mRNA(S1: 620 - 626个基点,S2: 1016 - 1022个基点),和一个荧光素酶分析显示,直接mir - 302 a有针对性的S1和S2。前体显著增强的表现减少COUP-TFII成骨的标记基因信使rna和蛋白质水平,碱性磷酸酶矿化活动和矩阵。一方面,显著抑制mir - 302 a减毒BMP2-induced成骨细胞特定的基因表情,碱性磷酸酶活性,矩阵与增加COUP-TFII矿化信使rna和蛋白质水平。mir - 302 a是诱导成骨的刺激和促进成骨细胞分化针对COUP-TFII。监管机构对成骨细胞分化。2014年威利期刊、公司。

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