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Status |
Public on May 09, 2016 |
Title |
5-hydroxymethylcytosine-mediated alteration of transposon activity associated with Preeclampsia |
Organism |
Homo sapiens |
Experiment type |
Methylation profiling by high throughput sequencing
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Summary |
Preeclampsia and gestational diabetes mellitus (GDM) are two of the most common clinical conditions during pregnancy that could result in adverse utero environments of the fetus. Fetal exposure to poor environments in uterus also raises the risk of future adulthood disorders known as fetal origins of adult disease (FOAD). Epigenetic modifications like cytosine methylation and histone modification have been proposed to be involved in FOAD. Recent research has implicated 5-hydroxymethylcytosine (5hmC), a DNA base derived from 5-methylcytosine (5mC) via oxidation by ten-eleven translocation (Tet) enzymes, in DNA methylation-related plasticity. Here we show that the expression of Tet2 and 5hmC abundance significantly altered in the umbilical vessels of preeclampsia. Genome-wide profiling of 5hmC revealed differentially hydroxymethylated regions (DhMRs) associated with preeclampsia and GDM, and DhMRs were enriched among the genes involved in unique biological pathways for each condition. In particular, 5hmC significantly changed in selective transposons and led to the alteration of transposon activity in preeclampsia. The 5hmC-mediated alteration of transposon activity was further confirmed using established hypoxia cell culture model and could be rescued by Vitamin C, a known activator of Tet proteins. Together our results suggest that adverse utero environments induced by preeclampsia could influence 5hmC-mediated epigenetic profile and contribute to FOAD.
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Overall design |
To determine the genome-wide 5hmC distribution in the the umbilical vessels of control, preeclampsia and GDM, we employed a previously established chemical labeling and affinity purification method, coupled with high-throughput sequencing (Song et al, Nature Biotechnology, 2011).
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Contributor(s) |
Jin P, Sun M |
Citation(s) |
27005421 |
Submission date |
Dec 11, 2015 |
Last update date |
May 15, 2019 |
Contact name |
Peng Jin |
E-mail(s) |
peng.jin@emory.edu
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Phone |
4047273729
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Organization name |
Emory University
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Department |
Human Genetics
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Lab |
Jin Lab
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Street address |
615 Michael St., Rm 325
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City |
Atlanta |
State/province |
Georgia |
ZIP/Postal code |
30322 |
Country |
USA |
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Platforms (1) |
GPL9052 |
Illumina Genome Analyzer (Homo sapiens) |
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Samples (3) |
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Relations |
BioProject |
PRJNA305754 |
SRA |
SRP067279 |
Supplementary file |
Size |
Download |
File type/resource |
GSE75941_RAW.tar |
4.1 Mb |
(http)(custom) |
TAR (of BED) |
SRA Run Selector |
Raw data are available in SRA |
Processed data provided as supplementary file |
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