Background: Maternal exposure to air pollution is associated with reduced fetal growth, but its relationship with expression of placental imprinted genes (important regulators of fetal growth) has not yet been studied.
Objectives: To examine relationships between maternal residential air pollution and expression of placental imprinted genes in the Rhode Island Child Health Study (RICHS).
Methods: Women-infant pairs were enrolled following delivery between 2009 and 2013. We geocoded maternal residential addresses at delivery, estimated daily levels of fine particulate matter (PM; n=355) and black carbon (BC; n=336) using spatial-temporal models, and estimated residential distance to nearest major roadway (n=355). Using linear regression models we investigated the associations between each exposure metric and expression of nine candidate genes previously associated with infant birthweight in RICHS, with secondary analyses of a panel of 108 imprinted genes expressed in the placenta. We also explored effect measure modification by infant sex.
Results: PM and BC were associated with altered expression for seven and one candidate genes, respectively, previously linked with birthweight in this cohort. Adjusting for multiple comparisons, we found that PM and BC were associated with changes in expression of 41 and 12 of 108 placental imprinted genes, respectively. Infant sex modified the association between PM and expression of CHD7 and between proximity to major roadways and expression of ZDBF2.
Conclusions: We found that maternal exposure to residential PM and BC was associated with changes in placental imprinted gene expression, which suggests a plausible line of investigation of how air pollution affects fetal growth and development.
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http://dx.doi.org/10.1016/j.envint.2017.08.022 | DOI Listing |
Front Cell Dev Biol
December 2024
Institute of Experimental Genetics, Helmholtz Munich GmbH, German Research Center for Environmental Health, Neuherberg, Germany.
Sexual dimorphism involves distinct anatomical, physiological, behavioral, and developmental differences between males and females of the same species, influenced by factors prior to conception and during early development. These sex-specific traits contribute to varied phenotypes and individual disease risks within and across generations and understanding them is essential in mammalian studies. Hormones, sex chromosomes, and imprinted genes drive this dimorphism, with over half of quantitative traits in wildtype mice showing sex-based variation.
View Article and Find Full Text PDFCommun Med (Lond)
December 2024
Environmental Epigenetics Laboratory, Department of Medical and Clinical Genetics, Medicum, University of Helsinki, Helsinki, Finland.
Background: Assisted reproductive technology (ART) has been associated with increased risks for growth disturbance, disrupted imprinting as well as cardiovascular and metabolic disorders. However, the molecular mechanisms and whether they are a result of the ART procedures or the underlying subfertility are unknown.
Methods: We performed genome-wide DNA methylation (EPIC Illumina microarrays) and gene expression (mRNA sequencing) analyses for a total of 80 ART and 77 control placentas.
J Reprod Dev
December 2024
Animal Science and Technology College, Beijing University of Agriculture, Beijing 102206, China.
Insulin-like growth factor 2 (IGF2) is essential for cell growth and differentiation and functions through the IGF2 receptor (IGF2R) to regulate embryonic and placental development. Exosomes that are synthesized and released from cells and play important roles in embryogenesis and placental development rely on the IGF2R for sorting and transport. However, the role of the imprinted Igf2-Igr2r axis and exosomes in the co-regulation of early placental development remains unknown.
View Article and Find Full Text PDFJ Reprod Immunol
November 2024
Braude College of Engineering, Karmiel, Israel. Electronic address:
CD24 is a mucin-like glycoprotein expressed on trophoblast cells and endothelial tissue of first and third trimester placentas. As an immune suppressor, CD24 may contribute to maternal immune tolerance to the growing fetus. CD24 is known to interact with the sialic acid-binding immunoglobulin-type lectins (Siglecs), specifically siglec-10.
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