المؤلفون: Lee, Samantha, Sbihi, Hind, MacIsaac, Julia L., Balshaw, Robert, Ambalavanan, Amirthagowri, Subbarao, Padmaja, Mandhane, Piushkumar J., Moraes, Theo J., Turvey, Stuart E., Qingling Duan, Brauer, Michael, Brook, Jeffrey R., Kobor, Michael S., Jones, Meaghan J.

المصدر: Environmental Health Perspectives; Apr2024, Vol. 132 Issue 4, p047004-1-047004-15, 15p

مصطلحات موضوعية: ASTHMA risk factors, RISK assessment, STATISTICAL correlation, CROSS-sectional method, PRENATAL exposure delayed effects, RESEARCH funding, ACADEMIC medical centers, DATA analysis, SECONDARY analysis, EPIGENOMICS, PROBABILITY theory, MULTIPLE regression analysis, CELL physiology, QUESTIONNAIRES, DESCRIPTIVE statistics, ATTITUDES of mothers, DNA methylation, PRENATAL care, LONGITUDINAL method, GENE expression, ENVIRONMENTAL exposure, RESEARCH, MICROARRAY technology, RESEARCH methodology, ANALYSIS of variance, STATISTICS, NITROGEN oxides, DATA analysis software, PHENOTYPES

مصطلحات جغرافية: CANADA

مستخلص: BACKGROUND: Evidence suggests that prenatal air pollution exposure alters DNA methylation (DNAm), which could go on to affect long-term health. It remains unclear whether DNAm alterations present at birth persist through early life. Identifying persistent DNAm changes would provide greater insight into the molecular mechanisms contributing to the association of prenatal air pollution exposure with atopic diseases. OBJECTIVES: This study investigated DNAm differences associated with prenatal nitrogen dioxide (NO2) exposure (a surrogate measure of trafficrelated air pollution) at birth and 1 y of age and examined their role in atopic disease. We focused on regions showing persistent DNAm differences from birth to 1 y of age and regions uniquely associated with postnatal NO2 exposure. METHODS: Microarrays measured DNAm at birth and at 1 y of age for an atopy-enriched subset of Canadian Health Infant Longitudinal Development (CHILD) study participants. Individual and regional DNAm differences associated with prenatal NO2 (푛= 128) were identified, and their persistence at age 1 y were investigated using linear mixed effects models (푛= 124). Postnatal-specific DNAm differences (푛= 125) were isolated, and their association with NO2 in the first year of life was examined. Causal mediation investigated whether DNAm differences mediated associations between NO2 and age 1 y atopy or wheeze. Analyses were repeated using biological sex-stratified data. RESULTS: At birth (푛= 128), 18 regions of DNAm were associated with NO2, with several annotated to HOX genes. Some of these regions were specifically identified in males (푛= 73), but not females (푛= 55). The effect of prenatal NO2 across CpGs within altered regions persisted at 1 y of age. No significant mediation effects were identified. Sex-stratified analyses identified postnatal-specific DNAm alterations. DISCUSSION: Regional cord blood DNAm differences associated with prenatal NO2 persisted through at least the first year of life in CHILD participants. Some differences may represent sex-specific alterations, but replication in larger cohorts is needed. The early postnatal period remained a sensitive window to DNAm perturbations. [ABSTRACT FROM AUTHOR]

: Copyright of Environmental Health Perspectives is the property of National Institute of Environmental Health Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Jones, Meaghan J.^1,2, Moore, Sarah R.^1,2, Kobor, Michael S.^1,2,3

المصدر: Annual Review of Psychology. 2018, Vol. 69, p459-485. 27p.

مصطلحات موضوعية: MENTAL illness genetics, AGE distribution, DNA, EPIDEMIOLOGY, EXPERIMENTAL design, GENE expression, PSYCHOLOGY, SEX distribution, EFFECT sizes (Statistics), DNA methylation, SEQUENCE analysis, EPIGENOMICS

مستخلص: The interplay of genetically driven biological processes and environmental factors is a key driver of research questions spanning multiple areas of psychology. A nascent area of research focuses on the utility of epigenetic marks in capturing this intersection of genes and environment, as epigenetic mechanisms are both tightly linked to the genome and environmentally responsive. Advances over the past 10 years have allowed large-scale assessment of one epigenetic mark in particular, DNA methylation, in human populations, and the examination of DNA methylation is becoming increasingly common in psychological studies. In this review, we briefly outline some principles of epigenetics, focusing on highlighting important considerations unique to DNA methylation studies to guide psychologists in incorporating DNA methylation into a project. We discuss study design and biological and analytical considerations and conclude by discussing interpretability of epigenetic findings and how these important factors are currently being applied across areas of psychology. [ABSTRACT FROM AUTHOR]

: Copyright of Annual Review of Psychology is the property of Annual Reviews Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Clifford, Rachel L., Jones, Meaghan J.

المصدر: American Journal of Respiratory Cell & Molecular Biology; Oct2021, Vol. 65 Issue 4, p335-336, 2p

مصطلحات موضوعية: GOVERNMENT policy, GENE expression, DNA methylation, CIGARETTE smokers, TRANSCRIPTION factors

مستخلص: An editorial is presented on environmental exposures influencing health and policies reducing or eliminating the exposures. Topics include identifying gene expression and DNA methylation differences between current smokers and ex-smokersin nasal epithelium; replicating in external data of cultured bronchial epithelia exposed to cigarette smoke; and smoking-related DNA methylation changes to transcription factor binding and subsequent changes in gene expression.