DNA methylation of the Rtl1 promoter in the placentas with fetal growth restriction.


Journal

Pediatrics and neonatology
ISSN: 2212-1692
Titre abrégé: Pediatr Neonatol
Pays: Singapore
ID NLM: 101484755

Informations de publication

Date de publication:
10 2019
Historique:
received: 21 08 2018
revised: 03 10 2018
accepted: 02 01 2019
pubmed: 27 1 2019
medline: 15 4 2020
entrez: 26 1 2019
Statut: ppublish

Résumé

Small for gestational age (SGA) babies experience fetal growth restriction because of placental insufficiency, and aberrant fetal growth has been linked to DNA methylation in the placenta. An imprinted gene encoding retrotransposon-like protein 1 (RTL1) is regulated by DNA methylation in the promoter region and plays a key role in placental development. We therefore investigated the DNA methylation status of RTL1 in the placenta of infants with severe SGA. We extracted DNA from the placenta of appropriate for gestational age (AGA; gestational age 35 ± 6 weeks, birthweight 2292 ± 1006 g; n = 12), SGA (birthweight z-score ≤-2 SD, 33 ± 5 weeks, 1373 ± 580 g; n = 11), and severe SGA (birthweight z-score ≤-3 SD, 33 ± 4 weeks, 1145 g ± 423 g; n = 7) infants, and we determined the methylation rates of five CpG sites in the CG4 (82,275,427-82,275,737 in NT_026437 sequence, NCBI database) region of the RTL1 promoter by pyrosequencing. We defined hypermethylation (>75.5%) and hypomethylation (<45.6%) based on the average methylation rate exceeding ± two standard deviations (SD) in the AGA group, respectively, and compared these among groups. There was no significant difference in the average methylation of CpG1-5 (control 59%, SGA 60%, severe SGA 63%), but abnormal methylation (hyper-/hypo-methylation) in CpG1 differed significantly among the groups (control 0%, SGA 36%, severe SGA 71%). Infants with severe SGA have abnormal placental DNA methylation of CpG1 in the CG4 region of RTL1, suggesting the existence of disturbed epigenetic control in utero.

Sections du résumé

BACKGROUND
Small for gestational age (SGA) babies experience fetal growth restriction because of placental insufficiency, and aberrant fetal growth has been linked to DNA methylation in the placenta. An imprinted gene encoding retrotransposon-like protein 1 (RTL1) is regulated by DNA methylation in the promoter region and plays a key role in placental development. We therefore investigated the DNA methylation status of RTL1 in the placenta of infants with severe SGA.
METHODS
We extracted DNA from the placenta of appropriate for gestational age (AGA; gestational age 35 ± 6 weeks, birthweight 2292 ± 1006 g; n = 12), SGA (birthweight z-score ≤-2 SD, 33 ± 5 weeks, 1373 ± 580 g; n = 11), and severe SGA (birthweight z-score ≤-3 SD, 33 ± 4 weeks, 1145 g ± 423 g; n = 7) infants, and we determined the methylation rates of five CpG sites in the CG4 (82,275,427-82,275,737 in NT_026437 sequence, NCBI database) region of the RTL1 promoter by pyrosequencing. We defined hypermethylation (>75.5%) and hypomethylation (<45.6%) based on the average methylation rate exceeding ± two standard deviations (SD) in the AGA group, respectively, and compared these among groups.
RESULTS
There was no significant difference in the average methylation of CpG1-5 (control 59%, SGA 60%, severe SGA 63%), but abnormal methylation (hyper-/hypo-methylation) in CpG1 differed significantly among the groups (control 0%, SGA 36%, severe SGA 71%).
CONCLUSION
Infants with severe SGA have abnormal placental DNA methylation of CpG1 in the CG4 region of RTL1, suggesting the existence of disturbed epigenetic control in utero.

Identifiants

pubmed: 30679037
pii: S1875-9572(18)30550-3
doi: 10.1016/j.pedneo.2019.01.001
pii:
doi:

Substances chimiques

Pregnancy Proteins 0
RTL1 protein, human 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

512-516

Informations de copyright

Copyright © 2019. Published by Elsevier B.V.

Auteurs

Kazumichi Fujioka (K)

Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan. Electronic address: fujiokak@med.kobe-u.ac.jp.

Kosuke Nishida (K)

Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan.

Mariko Ashina (M)

Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan.

Shinya Abe (S)

Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan.

Sachiyo Fukushima (S)

Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan.

Toshihiko Ikuta (T)

Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan.

Shohei Ohyama (S)

Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan.

Ichiro Morioka (I)

Department of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan.

Kazumoto Iijima (K)

Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan.

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Classifications MeSH