Gestational age acceleration is associated with epigenetic biomarkers of prenatal physiologic stress exposure
Carregando...
Citações na Scopus
3
Tipo de produção
article
Data de publicação
2022
Título da Revista
ISSN da Revista
Título do Volume
Editora
BMC
Autores
FELTRIN, Arthur Sant'Anna
FINK, Gunther
Citação
CLINICAL EPIGENETICS, v.14, n.1, article ID 152, 10p, 2022
Resumo
Background 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.
Palavras-chave
DNA methylation age, Gestational age acceleration, Prenatal psychosocial stress, Sex bias
Referências
- Barker ED, 2018, DEV PSYCHOPATHOL, V30, P1145, DOI 10.1017/S0954579418000330
- Binder AM, 2018, EPIGENETICS-US, V13, P85, DOI 10.1080/15592294.2017.1414127
- Bohlin J, 2016, GENOME BIOL, V17, DOI 10.1186/s13059-016-1063-4
- Braithwaite EC, 2018, J DEV ORIG HLTH DIS, V9, P425, DOI 10.1017/S2040174418000181
- Braithwaite EC, 2017, PHYSIOL BEHAV, V175, P31, DOI 10.1016/j.physbeh.2017.03.017
- Buurstede JC, 2022, NEUROPHARMACOLOGY, V216, DOI 10.1016/j.neuropharm.2022.109186
- Chen BH, 2016, AGING-US, V8, P1844, DOI 10.18632/aging.101020
- Danese A, 2017, ANNU REV PSYCHOL, V68, P517, DOI 10.1146/annurev-psych-010416-044208
- Dieckmann Linda, 2021, Clin Epigenetics, V13, P97, DOI 10.1186/s13148-021-01080-y
- Fransquet PD, 2019, CLIN EPIGENETICS, V11, DOI 10.1186/s13148-019-0656-7
- Girchenko P, 2017, CLIN EPIGENETICS, V9, DOI 10.1186/s13148-017-0349-z
- Han VX, 2021, NAT REV NEUROL, V17, P564, DOI 10.1038/s41582-021-00530-8
- Khouja JN, 2018, CLIN EPIGENETICS, V10, DOI 10.1186/s13148-018-0520-1
- Knight AK, 2018, J PEDIATR-US, V198, P168, DOI 10.1016/j.jpeds.2018.02.074
- Knight AK, 2016, GENOME BIOL, V17, DOI 10.1186/s13059-016-1068-z
- Koen N, 2021, TRANSL PSYCHIAT, V11, DOI 10.1038/s41398-021-01434-3
- Maschietto M, 2017, SCI REP-UK, V7, DOI 10.1038/srep44547
- McGill MG, 2022, BIOL PSYCHIAT, V91, P303, DOI 10.1016/j.biopsych.2021.07.025
- Moisiadis VG, 2014, NAT REV ENDOCRINOL, V10, P403, DOI 10.1038/nrendo.2014.74
- Moisiadis VG, 2014, NAT REV ENDOCRINOL, V10, P391, DOI 10.1038/nrendo.2014.73
- Money KM, 2018, MOL PSYCHIATR, V23, DOI 10.1038/mp.2017.191
- Oblak L, 2021, AGEING RES REV, V69, DOI 10.1016/j.arr.2021.101348
- Palma-Gudiel H, 2019, CLIN EPIGENETICS, V11, DOI 10.1186/s13148-019-0674-5
- Reed MD, 2020, NATURE, V577, P249, DOI 10.1038/s41586-019-1843-6
- Scheinost D, 2020, NEUROPSYCHOPHARMACOL, V45, P1272, DOI 10.1038/s41386-020-0677-0
- Schepanski S, 2018, FRONT IMMUNOL, V9, DOI 10.3389/fimmu.2018.02186
- Schroeder JW, 2011, EPIGENETICS-US, V6, P1498, DOI 10.4161/epi.6.12.18296
- Seale K, 2022, NAT REV GENET, V23, P585, DOI 10.1038/s41576-022-00477-6
- Solomon O, 2022, MUTAT RES-REV MUTAT, V789, DOI 10.1016/j.mrrev.2022.108415
- Suarez A, 2018, J AM ACAD CHILD PSY, V57, P321, DOI 10.1016/j.jaac.2018.02.011
- Zoubovsky SP, 2022, TRANSL PSYCHIAT, V12, DOI 10.1038/s41398-022-01785-5
Coleções
Artigos e Materiais de Revistas Científicas - FM/MOG
Artigos e Materiais de Revistas Científicas - FM/MPE
Artigos e Materiais de Revistas Científicas - FM/MPS
Artigos e Materiais de Revistas Científicas - FM/MPT
Artigos e Materiais de Revistas Científicas - HC/IPq
Artigos e Materiais de Revistas Científicas - HU
Carregar mais Artigos e Materiais de Revistas Científicas - FM/MPE
Artigos e Materiais de Revistas Científicas - FM/MPS
Artigos e Materiais de Revistas Científicas - FM/MPT
Artigos e Materiais de Revistas Científicas - HC/IPq
Artigos e Materiais de Revistas Científicas - HU