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PLAGL1甲基化水平和胎儿及出生后早期生长异常之间的关系:meta分析 被引量:2

The relationship between PLAGL1 methylation level and the risk of abnormal growth: a meta-analysis
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摘要 目的研究表明PLAGL1甲基化差异区域(differentiallymethylatedregion,OMR)的甲基化水平与一些生长障碍综合征相关。该文探讨PLAGL1DMR甲基化水平异常变化与胎儿以及出生后早期发育的关系。方法利用PubMed、Medline、EMBASE、万方数据库进行搜索,聚合生长障碍儿童与正常儿童之间PLAGL1 DMR甲基化的比较数据,进行系统的meta分析。结果共纳入文献7篇,涉及195例病例、438例对照和6种生长障碍性综合征。数据分析显示,生长异常(生长过剩或生长缺陷)组与对照组之间PLAGL1 DMR甲基化平均水平的差异为SMD=-1.05(95%C/为-1.93~0.17,P:0.02),结果显示生长异常儿童与正常组相比较,PLAGL1 DMR甲基化水平偏低,此差异有统计学意义。在此基础上,分析了生长异常组与正常组中PLAGL1DMR低甲基化的OR值,结果显示OR=2.18(95%C/为1.23—3.88,P=0.008)。结论PLAGL1的低甲基化是造成胎儿早期发育生长异常的一个风险因素。 Objective Studies and researches have indicated that the methylation level of PLAGL1 dif- ferentially methylated region (DMR) was associated with some development disorder syndromes. This project is purposed to prove whether methylation levels of PLAGL1 DMR is related to the fetal and early postnatal develop- ment. Methods We performed a meta-analysis of the published data on PLAGL1 DMR methylation levels in children with developmental disorders compared with that in normal children. Results PubMed, Medline, EM- BASE,WanFang databases were systematically searched to identify relevant studies. We included 7 studies in this meta-analysis,with a total of 195 cases and 438 controls concerning 6 kinds of developmental disorder syn- dromes. The methylation level of PLAGL1 DMR was lower in children with abnormal growth ( excess growth or retarded growth) than that in normal children,with a pooled percentage mean methylation difference (95% con- fidence intervals) of -1.05 (-1.93,-0. 17 ). On this basis, we analyzed the odds ratio (95% confidence inter- vals) of hypomethylation of PLAGL1 DMR in abnormal growth children in comparison with normal children. The combined odds ratio (95% confidence intervals) of hypomethylation in abnormal growth children is 2. 18 (1.23,3.88) in comparison with normal children. Conclusion Hypomethylation of PLALGI is actually a risk factor of suffering abnormal growth for children.
作者 辛雨 姚秀英 刘鑫丽 上宦少方 吴丽华 卢晓琳 常韶燕 王珍 张霆 王理 Xin Yu;Yao Xiuying;Liu Xinli;Shangguan'Shaofang;Wu Lihua;Lu Xiaolin;Chang Shaoyan;Wang Zhen;Zhang Ting;Wang Li(Beijing Municipal Key Laboratory of Child Development and Nutriomics , Capital Institute of Ped- iatrics .Beiiing 100020. China)
出处 《国际儿科学杂志》 2017年第12期872-876,881,共6页 International Journal of Pediatrics
基金 国家自然科学基金(81670802)
关键词 META分析 PLAGL1 差异性甲基化区域 甲基化 生长异常 Meta-analysis PLAGL1 Differentially methylated region Methylation Abnormal growth
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  • 1孔祥永,杜江,封志纯.甲状腺转录因子-1在人胎肺和新生儿肺上皮细胞中的时序表达[J].中国当代儿科杂志,2006,8(1):30-32. 被引量:3
  • 2李敏才,李娜萍,王曦.表面活性蛋白B、甲状腺转录因子在新生儿肺透明膜病中的表达及意义[J].临床儿科杂志,2007,25(3):198-200. 被引量:4
  • 3Harris MJ,Juriloff DM. An update to the list of mouse mutants withneural tube closure defects and advances toward a complete geneticperspective of neural tube closure[ J]. Birth Defects Res A Clin MolTeratol,2010,88(8) :653-669. DOI: 10. 1002/bdra. 20676.
  • 4Cai W,Zhao H ,Guo J,et al. Retinoic acid-induced lumbosacral neu-ral tube defects : myeloschisis and hamartoma [ J ]. Childs Nerv Syst,2007,23(5) :549-554.
  • 5Rohwedel J,Guan K, Wobus AM. Induction of cellular differentiationby retinoic acid in vitro[ J]. Cells Tissues Organs, 1999,165(3-4):190-202.
  • 6Jensen JB,Parmar M. Strengths and limitations of the neurosphereculture system[ J]. Mol Neurobiol,2006,34 (3) : 153-161. DOI : 10.1385/MN:34:3:153.
  • 7Galli-Resta L, Ensini M. An intrinsic time limit between genesis anddeath of individual neurons in the developing retinal ganglion celllayer[J]. J Neurosci, 1996,16(7) :2318-2324.
  • 8Oyadomari S, Mori M. Roles of CHOP/GADDI53 in endoplasmicreticulum stress[ J]. Cell Death Differ,2004,11(4):381-389. DOI:10. 1038/sj.cdd. 4401373.
  • 9Woo CW,Kutzler L, Kimball SR,et al. Toll-like receptor activationsuppresses ER stress factor CHOP and translation inhibition throughactivation of eIF2B[J]. Nat Cell Biol,2012,14(2) : 192-200. DOI:10. 1038/ncb2408.
  • 10Tanegashima K,Zhao H,Rebbert ML,et al. Coordinated activation ofthe secretory pathway during notochord formation in the Xenopusembryo[ J ]. Development, 2009, 136 ( 21 ) : 3543-3548. DOI : 10.1242/dev.036715.

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