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首页> 外文期刊>Journal of cellular biochemistry. >Hypoxia‐responsive miRNA‐21‐5p inhibits Runx2 suppression by targeting SMAD7 in MC3T3‐E1 cells
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Hypoxia‐responsive miRNA‐21‐5p inhibits Runx2 suppression by targeting SMAD7 in MC3T3‐E1 cells

机译：缺氧响应的miRNA-21-5P通过靶向MC3T3-E1细胞中的Smad7来抑制Runx2抑制

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Abstract Sustained hypoxia inhibits osteogenesis and osteoblast differentiation by downregulating the expression of runt‐related transcription factor 2 (Runx2). MicroRNAs (miRNAs) have been shown to regulate osteogenesis and osteoblast differentiation. In the present study, we profiled miRNAs, with microRNA array and quantitative real‐time polymerase chain reaction (RT‐PCR) methods, in mouse osteoblast (MC3T3‐E1) cells under hypoxia. Then, we investigated regulation by miRNA‐21‐5p on the expression of Runx2 and other osteoblast differentiation‐associated markers via gain‐of‐function and loss‐of‐function strategies. We found that expression of miRNA‐21‐5p, miRNA‐210‐5p, and other eight miRNAs was upregulated significantly in hypoxia‐treated MC3T3‐E1 cells. miRNA‐21‐5p overexpression downregulated the expression of the mRNA and protein of suppressor of mothers against decapentaplegic ( SMAD7 ) markedly, the 3′‐untranslated region (3′‐UTR) of which was highly homologous with the miRNA‐21‐5p sequence. miRNA‐21‐5p overexpression upregulated the protein expression of Runx2 in hypoxia‐treated?MC3T3‐E1 cells, although mRNA expression of Runx2 and other osteoblast differentiation‐associated molecules (eg, osteocalcin, procollagen type 1 amino‐terminal propeptide, P1NP) were not regulated by it; such upregulation was SMAD7‐dependent. In conclusion, hypoxia‐responsive miRNA‐21‐5p promoted Runx2 expression (at least in part) by targeting the 3′‐UTR and downregulating SMAD7 expression. Our study suggests a protective role of miRNA‐21‐5p in promoting osteoblast differentiation under hypoxia.
机译：摘要持续缺氧通过下调runt相关转录因子2（RUNX2）的表达来抑制成骨和成骨细胞分化。已经显示MicroRNAs（miRNA）调节骨性发生和成骨细胞分化。在本研究中，我们在缺氧下的小鼠成骨细胞（MC3T3-E1）细胞中具有MIRRNA阵列和定量实时聚合酶链反应（RT-PCR）方法的MIRNA。然后，我们通过函数增益和功能丧失策略来研究MiRNA-21-5P对runx2和其他成骨细胞分化相关标志物的调节。我们发现MiRNA-21-5P，MiRNA-210-5P和其他八个miRNA的表达在缺氧处理的MC3T3-E1细胞中显着上调。 miRNA-21-5P过表达下调了母亲抑制剂的mRNA和蛋白质的表达，其明显的3'-未翻译区域（3'-UTR）与miRNA-21-5P序列高度同源。 MiRNA-21-5P过表达上调了缺氧处理的αMC3T3-E1细胞中runx2的蛋白质表达，尽管Runx2和其他成骨细胞分化相关分子的mRNA表达（例如，骨甲酰蛋白，Procollagen型1氨基末端肽，P1NP）是不受它的监管;这种上调是Smad7依赖的。总之，通过靶向3'--UTR和下调Smad7表达，缺氧响应MiRNA-21-5P促进Runx2表达（至少部分）。我们的研究表明miRNA-21-5P在促进缺氧下促进成骨细胞分化方面的保护作用。

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