Genome-wide association study identifies a novel maternal gene × stress interaction associated with spontaneous preterm birth.

Adult Cohort Studies Female Genome-Wide Association Study Humans Infant, Newborn Infant, Premature Male Polymorphism, Single Nucleotide Pregnancy Stress, Physiological / genetics

Journal

Pediatric research
ISSN: 1530-0447
Titre abrégé: Pediatr Res
Pays: United States
ID NLM: 0100714

Informations de publication

Date de publication:
05 2021
Historique:
received: 11 03 2020
accepted: 27 06 2020
revised: 18 06 2020
pubmed: 30 7 2020
medline: 21 1 2022
entrez: 30 7 2020
Statut: ppublish

Résumé

Maternal stress is potentially a modifiable risk factor for spontaneous preterm birth (sPTB). However, epidemiologic findings on the maternal stress-sPTB relationship have been inconsistent. To investigate whether the maternal stress-sPTB associations may be modified by genetic susceptibility, we performed genome-wide gene × stress interaction analyses in 1490 African-American women from the Boston Birth cohort who delivered term (n = 1033) or preterm (n = 457) infants. Genotyping was performed using Illumina HumanOmni 2.5 array. Replication was performed using data from the NICHD genomic and Proteomic Network (GPN) for PTB research. rs35331017, a T-allele insertion/deletion polymorphism in the protein-tyrosine phosphatase receptor Type D (PTPRD) gene, was the top hit that interacted significantly with maternal lifetime stress on risk of sPTB (P We demonstrated a significant maternal PTPRD × stress interaction on sPTB risk. This finding, if further confirmed, may provide new insight into individual susceptibility to stress-induced sPTB. This was the first preterm study to demonstrate a significant genome-wide gene-stress interaction in African Americans, specifically, PTPRD gene variants can interact with maternal perceived stress to affect risk of spontaneous preterm birth. The PTPRD × maternal stress interaction was demonstrated in African Americans and replicated in both African Americans and Caucasians from the GPN study. Our findings highlight the importance of considering genetic susceptibility in assessing the role of maternal stress on spontaneous preterm birth.

Sections du résumé

BACKGROUND
Maternal stress is potentially a modifiable risk factor for spontaneous preterm birth (sPTB). However, epidemiologic findings on the maternal stress-sPTB relationship have been inconsistent.
METHODS
To investigate whether the maternal stress-sPTB associations may be modified by genetic susceptibility, we performed genome-wide gene × stress interaction analyses in 1490 African-American women from the Boston Birth cohort who delivered term (n = 1033) or preterm (n = 457) infants. Genotyping was performed using Illumina HumanOmni 2.5 array. Replication was performed using data from the NICHD genomic and Proteomic Network (GPN) for PTB research.
RESULTS
rs35331017, a T-allele insertion/deletion polymorphism in the protein-tyrosine phosphatase receptor Type D (PTPRD) gene, was the top hit that interacted significantly with maternal lifetime stress on risk of sPTB (P
CONCLUSION
We demonstrated a significant maternal PTPRD × stress interaction on sPTB risk. This finding, if further confirmed, may provide new insight into individual susceptibility to stress-induced sPTB.
IMPACT
This was the first preterm study to demonstrate a significant genome-wide gene-stress interaction in African Americans, specifically, PTPRD gene variants can interact with maternal perceived stress to affect risk of spontaneous preterm birth. The PTPRD × maternal stress interaction was demonstrated in African Americans and replicated in both African Americans and Caucasians from the GPN study. Our findings highlight the importance of considering genetic susceptibility in assessing the role of maternal stress on spontaneous preterm birth.

Identifiants

DOI: 10.1038/s41390-020-1093-1 PMID: 32726798 PMC: PMC8400921
pubmed: 32726798
doi: 10.1038/s41390-020-1093-1
pii: 10.1038/s41390-020-1093-1
pmc: PMC8400921
mid: NIHMS1724167
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

1549-1556

Subventions

Organisme : NICHD NIH HHS
ID : R24 HD042854
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201200008C
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD041702
Pays : United States
Organisme : NICHD NIH HHS
ID : R21 HD085556
Pays : United States
Organisme : NICHD NIH HHS
ID : R03 HD096136
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD086013
Pays : United States
Organisme : NICHD NIH HHS
ID : P2C HD042854
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201200008I
Pays : United States
Organisme : NCATS NIH HHS
ID : U54 TR001012
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD098232
Pays : United States

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Auteurs

Xiumei Hong (X)

Center on the Early Life Origins of Disease, Department of Population, Family and Reproductive Health, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA. xhong3@jhu.edu.

Pamela J Surkan (PJ)

Department of International Health, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.

Boyang Zhang (B)

Department of Biostatistics, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.

Amaris Keiser (A)

Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Yuelong Ji (Y)

Center on the Early Life Origins of Disease, Department of Population, Family and Reproductive Health, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.

Hongkai Ji (H)

Department of Biostatistics, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.

Irina Burd (I)

Integrated Research Center for Fetal Medicine, Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Blandine Bustamante-Helfrich (B)

Department of Clinical and Applied Science Education (Pathology), University of the Incarnate Word School of Osteopathic Medicine, San Antonio, TX, USA.

S Michelle Ogunwole (SM)

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Wan-Yee Tang (WY)

Department of Environmental Health and Engineering, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.

Li Liu (L)

Department of Population, Family and Reproductive Health, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.

Colleen Pearson (C)

Department of Pediatrics, Boston University School of Medicine and Boston Medical Center, Boston, MA, USA.

Sandra Cerda (S)

Department of Pathology and Laboratory Medicine, Boston Medical Center, Boston, MA, USA.

Barry Zuckerman (B)

Department of Pediatrics, Boston University School of Medicine and Boston Medical Center, Boston, MA, USA.

Lingxin Hao (L)

Department of Sociology, Johns Hopkins University, Baltimore, MD, USA.

Xiaobin Wang (X)

Center on the Early Life Origins of Disease, Department of Population, Family and Reproductive Health, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA.
Division of General Pediatrics & Adolescent Medicine, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

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