Gestational age acceleration is associated with epigenetic biomarkers of prenatal physiologic stress exposure

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorEUCLYDES, Veronica
dc.contributor.authorGOMES, Catarina
dc.contributor.authorGOUVEIA, Gisele
dc.contributor.authorGASTALDI, Vinicius Daguano
dc.contributor.authorFELTRIN, Arthur Sant'Anna
dc.contributor.authorCAMILO, Caroline
dc.contributor.authorVIEIRA, Rossana Pulcineli
dc.contributor.authorFELIPE-SILVA, Aloisio
dc.contributor.authorGRISI, Sandra
dc.contributor.authorFINK, Gunther
dc.contributor.authorBRENTANI, Alexandra
dc.contributor.authorBRENTANI, Helena
dc.date.accessioned2023-02-23T14:55:47Z
dc.date.available2023-02-23T14:55:47Z
dc.date.issued2022
dc.description.abstractBackground Physiological maternal stress response, such as imbalance in the glucocorticoid pathway and immune system seems to be mediated by DNA methylation (DNAm) and might translate intrauterine stress exposures into phenotypic changes in a sex-specific manner. DNAm in specific sites can also predict newborn gestational age and gestational age acceleration (GAA). GAA occurs when the predicted biological age is higher than the chronological age. In adults, poor health outcomes related to this deviance are well documented and raise questions for the interpretation and prediction in early stages of life. Boys seem to be more vulnerable to intrauterine stress exposure than girls; however, the mechanisms of adaptive sex-specific responses are still unclear. We hypothesize that intrauterine stress exposure is associated with GAA and could be different in boys and girls if inflammatory or glucocorticoid pathways exposure is considered. Results Using the Western Region Birth Cohort (ROC-Sao Paulo, Brazil) (n = 83), we calculated DNAm age and GAA from cord blood samples. Two epigenetic risk scores were calculated as an indirect proxy for low-grade inflammation (i-ePGS) and for glucocorticoid exposure (GES). Multivariate linear regression models were applied to investigate associations of GAA with prenatal exposures. The i-ePGS and GES were included in different models with the same co-variates considering sex interactions. The first multivariate model investigating inflammatory exposure (adj. R-2 = 0.31, p = < 0.001) showed that GAA was positively associated with i-ePGS (CI, 0.26-113.87, p = 0.049) and negative pregnancy-related feelings (CI, 0.04-0.48 p = 0.019). No sex interaction was observed. The second model investigating glucocorticoid exposure (adj. R-2 = 0.32, p = < 0.001) showed that the higher was the GAA was associated with a lower the lower was the GES in girls (CI, 0.04-2.55, p = 0.044). In both models, maternal self-reported mental disorder was negatively associated with GAA. Conclusion Prenatal epigenetic score of exposure to low-grade inflammatory was a predictor of GAA for both sexes. Glucocorticoid epigenetic score seems to be more important to GAA in girls. This study supports the evidence of sex-specificity in stress response, suggesting the glucocorticoid as a possible pathway adopted by girls to accelerate the maturation in an adverse condition.eng
dc.description.indexMEDLINE
dc.description.indexPubMed
dc.description.indexWoS
dc.description.indexScopus
dc.description.sponsorshipConselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
dc.description.sponsorshipCoordenacao de Aperfeicoamento de Pessoal de Nivel Superior-Brasil (CAPES) [001]
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2018/18560-6]
dc.identifier.citationCLINICAL EPIGENETICS, v.14, n.1, article ID 152, 10p, 2022
dc.identifier.doi10.1186/s13148-022-01374-9
dc.identifier.eissn1868-7083
dc.identifier.issn1868-7075
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/51547
dc.language.isoeng
dc.publisherBMCeng
dc.relation.ispartofClinical Epigenetics
dc.rightsopenAccesseng
dc.rights.holderCopyright BMCeng
dc.subjectDNA methylation ageeng
dc.subjectGestational age accelerationeng
dc.subjectPrenatal psychosocial stresseng
dc.subjectSex biaseng
dc.subject.otherfetaleng
dc.subject.otherglucocorticoidseng
dc.subject.othercortisoleng
dc.subject.otherhealtheng
dc.subject.otherchildeng
dc.subject.wosOncologyeng
dc.subject.wosGenetics & Heredityeng
dc.titleGestational age acceleration is associated with epigenetic biomarkers of prenatal physiologic stress exposureeng
dc.typearticleeng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
dspace.entity.typePublication
hcfmusp.affiliation.countrySuíça
hcfmusp.affiliation.countryisoch
hcfmusp.author.externalFELTRIN, Arthur Sant'Anna:Fed Univ ABC, Ctr Math Computat & Cognit, Sao Bernardo Do Campo, Brazil
hcfmusp.author.externalFINK, Gunther:Univ Basel, Swiss Trop & Publ Hlth Inst, Dept Epidmiol & Publ Hlth, Basel, Switzerland
hcfmusp.citation.scopus3
hcfmusp.contributor.author-fmusphcVERONICA LUIZA VALE EUCLYDES COLOVATI
hcfmusp.contributor.author-fmusphcCATARINA DOS SANTOS GOMES
hcfmusp.contributor.author-fmusphcGISELE RODRIGUES GOUVEIA
hcfmusp.contributor.author-fmusphcVINICIUS DAGUANO GASTALDI
hcfmusp.contributor.author-fmusphcCAROLINE PEREZ CAMILO
hcfmusp.contributor.author-fmusphcROSSANA PULCINELI VIEIRA FRANCISCO
hcfmusp.contributor.author-fmusphcALOISIO SOUZA FELIPE DA SILVA
hcfmusp.contributor.author-fmusphcSANDRA JOSEFINA FERRAZ ELLERO GRISI
hcfmusp.contributor.author-fmusphcALEXANDRA VALERIA MARIA BRENTANI
hcfmusp.contributor.author-fmusphcHELENA PAULA BRENTANI
hcfmusp.description.articlenumber152
hcfmusp.description.issue1
hcfmusp.description.volume14
hcfmusp.origemWOS
hcfmusp.origem.pubmed36443840
hcfmusp.origem.scopus2-s2.0-85142816964
hcfmusp.origem.wosWOS:000889558700003
hcfmusp.publisher.cityLONDONeng
hcfmusp.publisher.countryENGLANDeng
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hcfmusp.scopus.lastupdate2024-05-17
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