Methylation alterations of imprinted genes in different placental diseases.


Journal

Clinical epigenetics
ISSN: 1868-7083
Titre abrégé: Clin Epigenetics
Pays: Germany
ID NLM: 101516977

Informations de publication

Date de publication:
18 Sep 2024
Historique:
received: 24 05 2024
accepted: 30 08 2024
medline: 19 9 2024
pubmed: 19 9 2024
entrez: 18 9 2024
Statut: epublish

Résumé

Imprinted genes play important functions in placentation and pregnancy; however, research on their roles in different placental diseases is limited. It is believed that epigenetic alterations, such as DNA methylation, of placental imprinting genes may contribute to the different pathological features of severe placental diseases, such as pre-eclampsia (PE) and placenta accreta spectrum disorders (PAS). In this study, we conducted a comparative analysis of the methylation and expression of placental imprinted genes between PE and PAS using bisulfite sequencing polymerase chain reaction (PCR) and quantitative PCR, respectively. Additionally, we assessed oxidative damage of placental DNA by determining 8-hydroxy-2'-deoxyguanosine levels and fetal growth by determining insulin-like growth factor 2 (IGF2) and cortisol levels in the umbilical cord blood using enzyme-linked immunosorbent assay. Our results indicated that methylation and expression of potassium voltage-gated channel subfamily Q member 1, GNAS complex locus, mesoderm specific transcript, and IGF2 were significantly altered in both PE and PAS placentas. Additionally, our results revealed that the maternal imprinted genes were significantly over-expressed in PE and significantly under-expressed in PAS compared with a normal pregnancy. Moreover, DNA oxidative damage was elevated and positively correlated with IGF2 DNA methylation in both PE and PAS placentas, and cortisol and IGF2 levels were significantly decreased in PE and PAS. This study suggested that DNA methylation and expression of imprinted genes are aberrant in both PE and PAS placentas and that PE and PAS have different methylation profiles, which may be linked to their unique pathogenesis.

Sections du résumé

BACKGROUND BACKGROUND
Imprinted genes play important functions in placentation and pregnancy; however, research on their roles in different placental diseases is limited. It is believed that epigenetic alterations, such as DNA methylation, of placental imprinting genes may contribute to the different pathological features of severe placental diseases, such as pre-eclampsia (PE) and placenta accreta spectrum disorders (PAS).
RESULTS RESULTS
In this study, we conducted a comparative analysis of the methylation and expression of placental imprinted genes between PE and PAS using bisulfite sequencing polymerase chain reaction (PCR) and quantitative PCR, respectively. Additionally, we assessed oxidative damage of placental DNA by determining 8-hydroxy-2'-deoxyguanosine levels and fetal growth by determining insulin-like growth factor 2 (IGF2) and cortisol levels in the umbilical cord blood using enzyme-linked immunosorbent assay. Our results indicated that methylation and expression of potassium voltage-gated channel subfamily Q member 1, GNAS complex locus, mesoderm specific transcript, and IGF2 were significantly altered in both PE and PAS placentas. Additionally, our results revealed that the maternal imprinted genes were significantly over-expressed in PE and significantly under-expressed in PAS compared with a normal pregnancy. Moreover, DNA oxidative damage was elevated and positively correlated with IGF2 DNA methylation in both PE and PAS placentas, and cortisol and IGF2 levels were significantly decreased in PE and PAS.
CONCLUSIONS CONCLUSIONS
This study suggested that DNA methylation and expression of imprinted genes are aberrant in both PE and PAS placentas and that PE and PAS have different methylation profiles, which may be linked to their unique pathogenesis.

Identifiants

pubmed: 39294759
doi: 10.1186/s13148-024-01738-3
pii: 10.1186/s13148-024-01738-3
doi:

Substances chimiques

Insulin-Like Growth Factor II 67763-97-7
IGF2 protein, human 0
GTP-Binding Protein alpha Subunits, Gs EC 3.6.5.1
GNAS protein, human EC 3.6.1.-
Hydrocortisone WI4X0X7BPJ
mesoderm specific transcript protein 0
KCNQ1OT1 long non-coding RNA, human 0
Chromogranins 0
Proteins 0
Potassium Channels, Voltage-Gated 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

132

Subventions

Organisme : National Key Research and Development Program of China
ID : 2022YFC2704500
Organisme : Guangzhou Science, Technology and Innovation Commission
ID : SL2022A03J00860

Informations de copyright

© 2024. The Author(s).

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Auteurs

Xuwei Wang (X)

Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical University, No.63 Duobao Road, Liwan District, Guangzhou, 510150, Guangdong, China.
Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

Yunyun Liu (Y)

Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

Yuying Wu (Y)

The Third Clinical College of Guangzhou Medical University, Guangzhou, China.

Chunxi Lin (C)

The Third Clinical College of Guangzhou Medical University, Guangzhou, China.

Si Yang (S)

Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical University, No.63 Duobao Road, Liwan District, Guangzhou, 510150, Guangdong, China.
Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
BioResource Research Center, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

Yuhan Yang (Y)

Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical University, No.63 Duobao Road, Liwan District, Guangzhou, 510150, Guangdong, China.
Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

Dunjin Chen (D)

Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical University, No.63 Duobao Road, Liwan District, Guangzhou, 510150, Guangdong, China.
Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

Bolan Yu (B)

Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical University, No.63 Duobao Road, Liwan District, Guangzhou, 510150, Guangdong, China. yubolan-q@qq.com.
Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. yubolan-q@qq.com.
BioResource Research Center, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. yubolan-q@qq.com.

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