Evidence map›Paper›PMID 27005421›Full record

ArticleHuman molecular genetics2016

5-Hydroxymethylcytosine-mediated alteration of transposon activity associated with the exposure to adverse in utero environments in human.

Miao Sun, Mingxi M Song, Bin Wei, Qinqin Gao, Lingjun Li, Bing Yao, Li Chen, Li Lin, Qing Dai, Xiuwen Zhou and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 33 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 2 countries.

Miao SunInstitute for Fetology, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu 215006, China.
Mingxi M SongDepartment of Human Genetics, Emory University School of Medicine, Atlanta, GA 30322, USA.
Bin WeiInstitute for Fetology, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu 215006, China.
Qinqin GaoInstitute for Fetology, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu 215006, China.
Lingjun LiInstitute for Fetology, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu 215006, China.
Bing YaoDepartment of Human Genetics, Emory University School of Medicine, Atlanta, GA 30322, USA.
Li ChenDepartment of Human Genetics, Emory University School of Medicine, Atlanta, GA 30322, USA.
Li LinDepartment of Human Genetics, Emory University School of Medicine, Atlanta, GA 30322, USA.
Qing DaiDepartment of Chemistry, Department of Biochemistry and Molecular Biology, Institute for Biophysical Dynamics, Howard Hughes Medical Institute, The University of Chicago, Chicago, IL, USA.
Xiuwen ZhouInstitute for Fetology, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu 215006, China.
Jianying TaoInstitute for Fetology, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu 215006, China.
Jie ChenInstitute for Fetology, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu 215006, China.
Chuan HeDepartment of Chemistry, Department of Biochemistry and Molecular Biology, Institute for Biophysical Dynamics, Howard Hughes Medical Institute, The University of Chicago, Chicago, IL, USA.
Peng JinDepartment of Human Genetics, Emory University School of Medicine, Atlanta, GA 30322, USA peng.jin@emory.edu xuzhice@suda.edu.cn.
Zhice XuInstitute for Fetology, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu 215006, China peng.jin@emory.edu xuzhice@suda.edu.cn.
Emory University · USFirst Affiliated Hospital of Soochow University · CNSoochow University · CNHoward Hughes Medical Institute · USUniversity of Chicago · US

Funding

Tet-mediated Epigenetic Modulation in AutismR01MH102690 · NIMH · EMORY UNIVERSITY · PI JIN, PENG, WARREN, STEPHEN T. · 2014 to 2017
$2.6M
Collaborative Genetics Research Training ProgramD43TW006176 · FIC · JOHNS HOPKINS UNIVERSITY · PI JABS, ETHYLIN WANG · 2002 to 2006
$2.0M
5-Hydroxymethylcytosine in NeurodevelopmentR01NS079625 · NINDS · EMORY UNIVERSITY · PI JIN, PENG · 2012 to 2016
$1.7M
Investigation of 5-hmC, 5fC and 5-caC Modifications in Genome DNAK01HG006699 · NHGRI · UNIVERSITY OF CHICAGO · PI DAI, QING · 2012 to 2016
$702k
FIC NIH HHS D43 TW006176NHGRI NIH HHS K01 HG006699NIMH NIH HHS R01 MH102690NINDS NIH HHS R01 NS079625
6 · The paper itself

Abstract

Preeclampsia and gestational diabetes mellitus (GDM) are the most common clinical conditions in pregnancy that could result in adverse in utero environments. Fetal exposure to poor environments may raise the long-term risk of postnatal disorders, while epigenetic modifications could be involved. Recent research has implicated involvement of 5-hydroxymethylcytosine (5hmC), a DNA base derived from 5-methylcytosine, via oxidation by ten-eleven translocation (TET) enzymes, in DNA methylation-related plasticity. Here, we show that the TET2 expression and 5hmC abundance are significantly altered in the umbilical veins of GDM and preeclampsia. Genome-wide profiling of 5hmC revealed its specific reduction on intragenic regions from both GDM and preeclampsia compared to healthy controls. Gene Ontology analysis using loci bearing unique GDM- and preeclampsia-specific loss-of-5hmC indicated its impact on several critical biological pathways. Interestingly, the substantial alteration of 5hmC on several transposons and repetitive elements led to their differential expression. The alteration of TET expression, 5hmC levels and 5hmC-mediated transposon activity was further confirmed using established hypoxia cell culture model, which could be rescued by vitamin C, a known activator of TET proteins. Together, these results suggest that adverse pregnancy environments could influence 5hmC-mediated epigenetic profile and contribute to abnormal development of fetal vascular systems that may lead to postnatal diseases.

Indexed as

Epigenesis, Genetic5-MethylcytosineAdultAscorbic AcidDiabetes, GestationalDioxygenasesDNA-Binding ProteinsDNA MethylationDNA Transposable ElementsFemaleGene Expression Regulation, DevelopmentalHumansPre-EclampsiaPregnancyProto-Oncogene Proteins5-hydroxymethylcytosine5-MethylcytosineAscorbic AcidDioxygenasesDNA-Binding ProteinsDNA Transposable ElementsProto-Oncogene ProteinsTET2 protein, human

Identifiers

PMID27005421
PMCPMC5081053
OpenAlexW2307168987

What OpenQuestion holds

Textmetadata
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.