Genome-wide DNA methylation analysis of discordant monozygotic twins reveals consistent sites of differential methylation associated with congenital heart disease.


Journal

Genomics
ISSN: 1089-8646
Titre abrégé: Genomics
Pays: United States
ID NLM: 8800135

Informations de publication

Date de publication:
03 2023
Historique:
received: 01 10 2022
revised: 04 01 2023
accepted: 19 01 2023
pubmed: 24 1 2023
medline: 21 3 2023
entrez: 23 1 2023
Statut: ppublish

Résumé

Despite being essentially genetically identical, monozygotic (MZ) twins can be discordant for congenital heart disease (CHD), thus highlighting the importance of in utero environmental factors for CHD pathogenesis. This study aimed to identify the epigenetic variations between discordant MZ twin pairs that are associated with CHD at birth. Cord blood of CHD-discordant MZ twins from the Chongqing Longitudinal Twin Study Cohort was subjected to whole-genome bisulfite sequencing, then validated by MeDIP-qPCR and qRT-PCR. 379 DMRs mapped to 175 differentially methylated genes (DMGs) were associated with CHD. Functional enrichment analysis identified these DMGs are involved in histone methylation, actin cytoskeleton organization, the regulation of cell differentiation, and adrenergic signaling in cardiomyocytes. Of note, SPESP1 and NOX5 were hypermethylated in CHD, and associated with lower gene expression levels. Specific DNA methy (DNAm) variations in cord blood were associated with CHD, thus illustrating new biomarkers and potential interventional targets for CHD. ChiCTR-OOC-16008203, registered on 1 April 2016 at the Chinese Clinical Trial Registry.

Sections du résumé

BACKGROUND
Despite being essentially genetically identical, monozygotic (MZ) twins can be discordant for congenital heart disease (CHD), thus highlighting the importance of in utero environmental factors for CHD pathogenesis. This study aimed to identify the epigenetic variations between discordant MZ twin pairs that are associated with CHD at birth.
METHODS
Cord blood of CHD-discordant MZ twins from the Chongqing Longitudinal Twin Study Cohort was subjected to whole-genome bisulfite sequencing, then validated by MeDIP-qPCR and qRT-PCR.
RESULTS
379 DMRs mapped to 175 differentially methylated genes (DMGs) were associated with CHD. Functional enrichment analysis identified these DMGs are involved in histone methylation, actin cytoskeleton organization, the regulation of cell differentiation, and adrenergic signaling in cardiomyocytes. Of note, SPESP1 and NOX5 were hypermethylated in CHD, and associated with lower gene expression levels.
CONCLUSIONS
Specific DNA methy (DNAm) variations in cord blood were associated with CHD, thus illustrating new biomarkers and potential interventional targets for CHD.
TRIAL REGISTRATION
ChiCTR-OOC-16008203, registered on 1 April 2016 at the Chinese Clinical Trial Registry.

Identifiants

pubmed: 36690264
pii: S0888-7543(23)00009-5
doi: 10.1016/j.ygeno.2023.110565
pii:
doi:

Banques de données

ChiCTR
['ChiCTR-OOC-16008203']

Types de publication

Twin Study Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

110565

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Xi Yuan (X)

State Key Laboratory of Maternal and Fetal Medicine of Chongqing Municipality, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Jiayu Huang (J)

Reproductive Medicine Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Li Wen (L)

State Key Laboratory of Maternal and Fetal Medicine of Chongqing Municipality, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Boris Novakovic (B)

Molecular Immunity, Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne, Victoria, Australia; Department of Pediatrics, University of Melbourne, Parkville, VIC, Australia.

Mark D Kilby (MD)

Fetal Medicine Centre, Birmingham Women's & Children's Foundation Trust, Birmingham B15 2TG, UK; Institute of Metabolism & Systems Research, College of Medical & Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK.

Chao Tong (C)

State Key Laboratory of Maternal and Fetal Medicine of Chongqing Municipality, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. Electronic address: chaotongcqmu@163.com.

Hongbo Qi (H)

State Key Laboratory of Maternal and Fetal Medicine of Chongqing Municipality, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China; Department of Obstetrics, Women and Children's Hospital of Chongqing Medical University, Chongqing 401147, China. Electronic address: qihongbo728@163.com.

Richard Saffery (R)

Molecular Immunity, Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne, Victoria, Australia; Department of Pediatrics, University of Melbourne, Parkville, VIC, Australia. Electronic address: richard.saffery@mcri.edu.au.

Philip N Baker (PN)

State Key Laboratory of Maternal and Fetal Medicine of Chongqing Municipality, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China; College of Life Sciences, University of Leicester, Leicester LE1 7RH, UK. Electronic address: philip.baker@leicester.ac.uk.

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Classifications MeSH