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首页> 外文期刊>Journal of Molecular Biology >Post-Transcriptional Regulation of Renalase Gene by miR-29 and miR-146 MicroRNAs: Implications for Cardiometabolic Disorders
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Post-Transcriptional Regulation of Renalase Gene by miR-29 and miR-146 MicroRNAs: Implications for Cardiometabolic Disorders

机译：转录酶后转录调节的miR-29和miR-146 MicroRNA：对心脏代谢紊乱的影响。

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Renalase, a recently identified oxidoreductase, is emerging as a novel regulator of cardiovascular and metabolic disease states. The mechanism of regulation of renalase gene, especially at the post-transcriptional level, is completely unknown. We set out to investigate the possible role of nnicroRNAs in regulation of renalase gene in this study. Computational predictions using multiple algorithms coupled with systematic functional analysis revealed specific interactions of miR-29a/b/c and miR-146a/b with mouse and human renalase 3'-UTR (untranslated region) in cultured cells. Next, we estimated miR-29b and miR-146a, as well as renalase expression, in genetically hypertensive blood pressure high and genetically hypotensive blood pressure low mice. Kidney tissues from blood pressure high mice showed diminished (similar to 1.6- to 1.8-fold) renalase mRNA/protein levels and elevated (similar to 2.2-fold) miR-29b levels as compared to blood pressure low mice. A common single nucleotide polymorphism in human renalase 3'-UTR (UT; rs10749571) creates a binding site for miR-146a; consistently, miR-146a down-regulated human renalase 3'-UTR/luciferase activity in case of the T allele suggesting its potential role in regulation of renalase in humans. Indeed, genome-wide association studies revealed directionally concordant association of rs10749571 with diastolic blood pressure, glucose and triglyceride levels in large human populations (n approximate to 58,000-96,000 subjects). This study provides evidence for post-transcriptional regulation of renalase gene by miR-29 and miR-146 and has implications for inter-individual variations on cardiometabolic traits. (C) 2015 Elsevier Ltd. All rights reserved.
机译：肾病酶是一种最近发现的氧化还原酶，它正在成为心血管和代谢疾病状态的新型调节剂。肾酶基因的调节机制，特别是在转录后水平，是完全未知的。在此研究中，我们着手研究nnicroRNA在调节肾酶基因中的可能作用。使用多种算法的计算预测与系统的功能分析相结合，揭示了miR-29a / b / c和miR-146a / b与培养细胞中小鼠和人类肾酶3'-UTR（非翻译区）的特异性相互作用。接下来，我们估计了遗传性高血压和遗传性高血压的小鼠中miR-29b和miR-146a以及肾酶的表达。与低血压小鼠相比，来自高血压小鼠的肾脏组织显示肾酶mRNA /蛋白质水平降低（约1.6至1.8倍），miR-29b水平升高（约2.2倍）。人肾酶3'-UTR（UT; rs10749571）中常见的单核苷酸多态性产生了miR-146a的结合位点;一致地，在T等位基因的情况下，miR-146a下调了人类肾酶3'-UTR /荧光素酶的活性，表明其在调节人类肾酶中的潜在作用。实际上，全基因组关联研究显示，rs10749571与大型人群（n约为58,000-96,000名受试者）的舒张压，葡萄糖和甘油三酯水平在方向上一致相关。这项研究为miR-29和miR-146对肾酶基因的转录后调控提供了证据，并且对心脏代谢特性的个体间差异具有影响。 （C）2015 Elsevier Ltd.保留所有权利。

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