摘要
糖皮质激素 (GCs)通过由NR3C1基因编码的胞质糖皮质激素受体活化后,调节其基因表达发挥作用。导致GR自动调节的负反馈机制被证明是通过将激活的受体结合到包含在GR基因内叫做GRE样元素的基因内序列上。长非编码RNA生长停滞特异性转录5(GAS5)与活化的G5相互作用抑制其转录活性。本研究的目的是评价GAS5 和NR3C1基因在甲泼尼龙在外周血单核细胞的抗增殖作用中表达的可能作用,并关联该表达和个体对GCs的敏感性。对GC响应较弱的个体相比响应较强的个体表现出更高的GAS5和NR3C1水平。我们提出GAS5水平的异常可能会改变GC的效果,可能干扰GR自主调节机制。
关键词: GAS5,基因表达,糖皮质激素受体,长非编码RNA,甲泼尼龙,NR3C1基因,增殖活性。
Current Molecular Medicine
Title:Long Noncoding RNA GAS5: A Novel Marker Involved in Glucocorticoid Response
Volume: 15 Issue: 1
Author(s): M. Lucafo, S. De Iudicibus, A. Di Silvestre, M. Pelin, L. Candussio, S. Martelossi, A. Tommasini, E. Piscianz, A. Ventura and G. Decorti
Affiliation:
关键词: GAS5,基因表达,糖皮质激素受体,长非编码RNA,甲泼尼龙,NR3C1基因,增殖活性。
摘要: Glucocorticoids (GCs) exert their effects through regulation of gene expression after activation in the cytoplasm of the glucocorticoid receptor (GR) encoded by NR3C1 gene. A negative feedback mechanism resulting in GR autoregulation has been demonstrated through the binding of the activated receptor to intragenic sequences called GRE-like elements, contained in GR gene.
The long noncoding RNA growth arrest–specific transcript 5 (GAS5) interacts with the activated GR suppressing its transcriptional activity. The aim of this study was to evaluate the possible role of GAS5 and NR3C1 gene expression in the antiproliferative effect of methylprednisolone in peripheral blood mononuclear cells and to correlate the expression with individual sensitivity to GCs. Subjects being poor responders to GCs presented higher levels of GAS5 and NR3C1 in comparison with good responders. We suggest that abnormal levels of GAS5 may alter GC effectiveness, probably interfering with the mechanism of GR autoregulation.
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M. Lucafo, S. De Iudicibus, A. Di Silvestre, M. Pelin, L. Candussio, S. Martelossi, A. Tommasini, E. Piscianz, A. Ventura and G. Decorti , Long Noncoding RNA GAS5: A Novel Marker Involved in Glucocorticoid Response, Current Molecular Medicine 2015; 15 (1) . https://dx.doi.org/10.2174/1566524015666150114122354
DOI https://dx.doi.org/10.2174/1566524015666150114122354 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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