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      Patterning in Placental 11-B Hydroxysteroid Dehydrogenase Methylation According to Prenatal Socioeconomic Adversity

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          Abstract

          Background

          Prenatal socioeconomic adversity as an intrauterine exposure is associated with a range of perinatal outcomes although the explanatory mechanisms are not well understood. The development of the fetus can be shaped by the intrauterine environment through alterations in the function of the placenta. In the placenta, the HSD11B2 gene encodes the 11-beta hydroxysteroid dehydrogenase enzyme, which is responsible for the inactivation of maternal cortisol thereby protecting the developing fetus from this exposure. This gene is regulated by DNA methylation, and this methylation and the expression it controls has been shown to be susceptible to a variety of stressors from the maternal environment. The association of prenatal socioeconomic adversity and placental HSD11B2 methylation has not been examined. Following a developmental origins of disease framework, prenatal socioeconomic adversity may alter fetal response to the postnatal environment through functional epigenetic alterations in the placenta. Therefore, we hypothesized that prenatal socioeconomic adversity would be associated with less HSD11B2 methylation.

          Methods and Findings

          We examined the association between DNA methylation of the HSD11B2 promoter region in the placenta of 444 healthy term newborn infants and several markers of prenatal socioeconomic adversity: maternal education, poverty, dwelling crowding, tobacco use and cumulative risk. We also examined whether such associations were sex-specific. We found that infants whose mothers experienced the greatest levels of socioeconomic adversity during pregnancy had the lowest extent of placental HSD11B2 methylation, particularly for males. Associations were maintained for maternal education when adjusting for confounders (p<0.05).

          Conclusions

          Patterns of HSD11B2 methylation suggest that environmental cues transmitted from the mother during gestation may program the developing fetus’s response to an adverse postnatal environment, potentially via less exposure to cortisol during development. Less methylation of placental HSD11B2 may therefore be adaptive and promote the effective management of stress associated with social adversity in a postnatal environment.

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          Most cited references 26

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          Epigenetic programming by maternal behavior.

          Here we report that increased pup licking and grooming (LG) and arched-back nursing (ABN) by rat mothers altered the offspring epigenome at a glucocorticoid receptor (GR) gene promoter in the hippocampus. Offspring of mothers that showed high levels of LG and ABN were found to have differences in DNA methylation, as compared to offspring of 'low-LG-ABN' mothers. These differences emerged over the first week of life, were reversed with cross-fostering, persisted into adulthood and were associated with altered histone acetylation and transcription factor (NGFI-A) binding to the GR promoter. Central infusion of a histone deacetylase inhibitor removed the group differences in histone acetylation, DNA methylation, NGFI-A binding, GR expression and hypothalamic-pituitary-adrenal (HPA) responses to stress, suggesting a causal relation among epigenomic state, GR expression and the maternal effect on stress responses in the offspring. Thus we show that an epigenomic state of a gene can be established through behavioral programming, and it is potentially reversible.
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            The lasting impact of childhood health and circumstance.

            We quantify the lasting effects of childhood health and economic circumstances on adult health, employment and socioeconomic status, using data from a birth cohort that has been followed from birth into middle age. Controlling for parental income, education and social class, children who experience poor health have significantly lower educational attainment, poorer health, and lower social status as adults. Childhood health and circumstance appear to operate both through their impact on initial adult health and economic status, and through a continuing direct effect of prenatal and childhood health in middle age. Overall, our findings suggest more attention be paid to health as a potential mechanism through which intergenerational transmission of economic status takes place: cohort members born into poorer families experienced poorer childhood health, lower investments in human capital and poorer health in early adulthood, all of which are associated with lower earnings in middle age-the years in which they themselves become parents.
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              Socioeconomic status and health. The challenge of the gradient.

               N Adler,  S Boyce,  M Chesney (1993)
              Socioeconomic status (SES) is consistently associated with health outcomes, yet little is known about the psychosocial and behavioral mechanisms that might explain this association. Researchers usually control for SES rather than examine it. When it is studied, only effects of lower, poverty-level SES are generally examined. However, there is evidence of a graded association with health at all levels of SES, an observation that requires new thought about domains through which SES may exert its health effects. Variables are highlighted that show a graded relationship with both SES and health to provide examples of possible pathways between SES and health end points. Examples are also given of new analytic approaches that can better illuminate the complexities of the SES-health gradient.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                1932-6203
                2013
                5 September 2013
                : 8
                : 9
                Affiliations
                [1 ]Department of Community and Family Medicine, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America
                [2 ]Department of Pharmacology and Toxicology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America
                [3 ]Department of Pediatrics, Women and Infants Hospital, Providence, Rhode Island, United States of America
                [4 ]Brown Center for the Study of Children at Risk, Women and Infants Hospital, Providence, Rhode Island, United States of America
                King Faisal Specialist Hospital & Research center, Saudi Arabia
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: AAA DAA CJM. Performed the experiments: DAA CL. Analyzed the data: AAA DAA CJM. Contributed reagents/materials/analysis tools: DAA CL JL. Wrote the paper: AAA DAA CL JL JFP BML CJM.

                Article
                PONE-D-13-08852
                10.1371/journal.pone.0074691
                3764127
                24040322

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                Page count
                Pages: 7
                Funding
                Funding Sources: NIH-NIMH R01MH094609, NIH-NIGMS P20GM103537, NIH-NCI R25CA134286. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article

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