Hao Ruixin, Su Shengzhong, Wan Yinan, Shen Frank, Niu Ben, Coslo Denise M, Albert Istvan, Han Xing, Omiecinski Curtis J
DuPont Haskell Global Centers for Health and Environmental Sciences, Newark, Delaware, United States; Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA, United States.
Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA, United States.
Biochim Biophys Acta. 2016 Sep;1859(9):1228-1237. doi: 10.1016/j.bbagrm.2016.04.002. Epub 2016 Apr 11.
The constitutive androstane receptor (CAR; NR1I3) is a member of the nuclear receptor superfamily that functions as a xenosensor, serving to regulate xenobiotic detoxification, lipid homeostasis and energy metabolism. CAR activation is also a key contributor to the development of chemical hepatocarcinogenesis in mice. The underlying pathways affected by CAR in these processes are complex and not fully elucidated. MicroRNAs (miRNAs) have emerged as critical modulators of gene expression and appear to impact many cellular pathways, including those involved in chemical detoxification and liver tumor development. In this study, we used deep sequencing approaches with an Illumina HiSeq platform to differentially profile microRNA expression patterns in livers from wild type C57BL/6J mice following CAR activation with the mouse CAR-specific ligand activator, 1,4-bis-[2-(3,5,-dichloropyridyloxy)] benzene (TCPOBOP). Bioinformatic analyses and pathway evaluations were performed leading to the identification of 51 miRNAs whose expression levels were significantly altered by TCPOBOP treatment, including mmu-miR-802-5p and miR-485-3p. Ingenuity Pathway Analysis of the differentially expressed microRNAs revealed altered effector pathways, including those involved in liver cell growth and proliferation. A functional network among CAR targeted genes and the affected microRNAs was constructed to illustrate how CAR modulation of microRNA expression may potentially mediate its biological role in mouse hepatocyte proliferation. This article is part of a Special Issue entitled: Xenobiotic nuclear receptors: New Tricks for An Old Dog, edited by Dr. Wen Xie.
组成型雄烷受体(CAR;NR1I3)是核受体超家族的成员,作为一种异源物传感器发挥作用,用于调节异源物解毒、脂质稳态和能量代谢。CAR激活也是小鼠化学性肝癌发生发展的关键因素。在这些过程中,受CAR影响的潜在途径很复杂,尚未完全阐明。微小RNA(miRNA)已成为基因表达的关键调节因子,似乎会影响许多细胞途径,包括那些参与化学解毒和肝脏肿瘤发展的途径。在本研究中,我们使用Illumina HiSeq平台的深度测序方法,对野生型C57BL/6J小鼠肝脏在用小鼠CAR特异性配体激活剂1,4-双-[2-(3,5-二氯吡啶氧基)]苯(TCPOBOP)激活CAR后,进行微小RNA表达模式的差异分析。进行了生物信息学分析和途径评估,从而鉴定出51种其表达水平因TCPOBOP处理而显著改变的miRNA,包括mmu-miR-802-5p和miR-485-3p。对差异表达的微小RNA进行的 Ingenuity Pathway Analysis揭示了效应途径的改变,包括那些参与肝细胞生长和增殖的途径。构建了CAR靶向基因与受影响的微小RNA之间的功能网络,以说明CAR对微小RNA表达的调节如何可能介导其在小鼠肝细胞增殖中的生物学作用。本文是名为:异源物核受体:老狗新把戏 的特刊的一部分,由谢文博士编辑。