Differential DNA methylation and PM<sub>2.5</sub> species in a 450K epigenome-wide association study

Dai, Lingzhen; Mehta, Amar; Mordukhovich, Irina; Just, Allan C.; Shen, Jincheng; Hou, Lifang; Koutrakis, Petros; Sparrow, David; Vokonas, Pantel; Baccarelli, Andrea A.; Schwartz, Joel

doi:10.1080/15592294.2016.1271853

Cited by 56 publications

(33 citation statements)

References 54 publications

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“…DNA of whole blood samples were collected between 1999 and 2013. As previously described [36,37], we used the QIAamp DNA Blood Kit (Qiagen, CA, USA) to extract DNA from buffy coat, and performed bisulfite conversion with the EZ-96 DNA Methylation Kit (Zymo Research, CA, USA). To minimize batch effects, we randomized chips across plates and randomized samples based on a 2-stage age-stratified algorithm so that age distributed similarly across chips and plates.…”

Section: Methodsmentioning

confidence: 99%

Accelerated DNA methylation age and the use of antihypertensive medication among older adults

Gao

Colicino

Shen

et al. 2018

Aging

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The discrepancy of DNA methylation age (DNAmAge) with chronological age (termed as age acceleration, AA) has been identified to be associated with many aging-related health outcomes including hypertension. Since taking antihypertensive medication (AHM) could prevent aging-related diseases caused by hypertension, we hypothesized that using AHM could also reduce the AA. We examined this hypothesis among 546 males aged 55–85 years by exploring the associations of AHM use with AA and its change rate (ΔAA) in two visits with a median follow-up of 3.86 years. Horvath DNAmAge was derived from DNA methylation profiles measured by Illumina HumanMethylation450 BeadChip and information on AHM use was collected by physician interview. A general decreasing pattern of AA was observed between the two visits. After the fully adjusting for potential covariates including hypertension, any AHM use showed a cross-sectional significant association with higher AA at each visit, as well as a longitudinal association with increased ΔAA between visits. Particularly, relative to participants who never took any AHM, individuals with continuous AHM use had a higher ΔAA of 0.6 year/chronological year. This finding underlines that DNAmAge and AA may not be able to capture the preventive effects of AHMs that reduce cardiovascular risks and mortality.

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Section: Methodsmentioning

confidence: 99%

Accelerated DNA methylation age and the use of antihypertensive medication among older adults

Gao

Colicino

Shen

et al. 2018

Aging

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“…The analysis was adjusted for confounding effects of age, sex, and disease status. As a consequence, to prevent an increase in Type I errors, Bonferroni correction was used to analyze specific haplogroup differences between the H and J variants . CpG sites were considered significantly differentially methylated if the Bonferroni‐adjusted P value was less than 0.05.…”

Section: Methodsmentioning

confidence: 99%

Differential Association of Mitochondrial DNA Haplogroups J and H With the Methylation Status of Articular Cartilage: Potential Role in Apoptosis and Metabolic and Developmental Processes

Cortés-Pereira

Fernández‐Tajes

Fernández-Moreno

et al. 2019

Arthritis & Rheumatology

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Objective. To analyze the influence of mitochondrial genome variation on the DNA methylome of articular cartilage. Methods. DNA methylation profiling was performed using data deposited in the NCBI Gene Expression Omnibus database (accession no. GSE43269). Data were obtained for 14 cartilage samples from subjects with haplogroup J and 20 cartilage samples from subjects with haplogroup H. Subsequent validation was performed in an independent subset of 7 subjects with haplogroup J and 9 with haplogroup H by RNA-seq. Correlated genes were validated by real-time polymerase chain reaction in an independent cohort of 12 subjects with haplogroup J and 12 with haplogroup H. Appropriate analyses were performed using R Bioconductor and qBasePlus software, and gene ontology analysis was conducted using DAVID version 6.8.Results. DNA methylation profiling revealed 538 differentially methylated loci, while whole-transcriptome profiling identified 2,384 differentially expressed genes, between cartilage samples from subjects with haplogroup H and those with haplogroup J. Seventeen genes showed an inverse correlation between methylation and expression. In terms of gene ontology, differences in correlations between methylation and expression were also detected between cartilage from subjects with haplogroup H and those with haplogroup J, highlighting a significantly enhanced apo ptotic process in cartilage from subjects with haplogroup H (P = 0.007 for methylation and P = 0.019 for expression) and repressed apoptotic process in cartilage from subjects with haplogroup J (P = 0.021 for methylation), as well as a significant enrichment of genes related to metabolic processes (P = 1.93 × 10 −4 for methylation and P = 6.79 x 10 −4 for expression) and regulation of gene expression (P = 0.012 for methylation) in cartilage from subjects with haplogroup H, and to developmental processes (P = 0.015 for methylation and P = 8.25 x 10 −12 for expression) in cartilage from subjects with haplogroup J.Conclusion. Mitochondrial DNA variation differentially associates with the methylation status of articular cartilage by acting on key mechanisms involved in osteoarthritis, such as apoptosis and metabolic and developmental processes.

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“…We observed that the effect of prenatal PM 2.5 exposure on placental mtDNA content was mediated for 54% by mitochondrial 12S RNA methylation and for 27% by mitochondrial D-loop methylation [49]. Although studies on mitochondrial epigenetics are still in its infancy, PM 2.5 exposure may be a potential candidate with important links to mitochondrial epigenetics [107].…”

Section: Interplay Of Oxidative Stress Epigenetics and The Air Pollmentioning

confidence: 99%

Air pollution-induced placental alterations: an interplay of oxidative stress, epigenetics, and the aging phenotype?

et al. 2019

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According to the "Developmental Origins of Health and Disease" (DOHaD) concept, the early-life environment is a critical period for fetal programming. Given the epidemiological evidence that air pollution exposure during pregnancy adversely affects newborn outcomes such as birth weight and preterm birth, there is a need to pay attention to underlying modes of action to better understand not only these air pollution-induced early health effects but also its later-life consequences. In this review, we give an overview of air pollution-induced placental molecular alterations observed in the ENVIRONAGE birth cohort and evaluate the existing evidence. In general, we showed that prenatal exposure to air pollution is associated with nitrosative stress and epigenetic alterations in the placenta. Adversely affected CpG targets were involved in cellular processes including DNA repair, circadian rhythm, and energy metabolism. For miRNA expression, specific air pollution exposure windows were associated with altered miR-20a, miR-21, miR-146a, and miR-222 expression. Early-life aging markers including telomere length and mitochondrial DNA content are associated with air pollution exposure during pregnancy. Previously, we proposed the air pollution-induced telomere-mitochondrial aging hypothesis with a direct link between telomeres and mitochondria. Here, we extend this view with a potential co-interaction of different biological mechanisms on the level of placental oxidative stress, epigenetics, aging, and energy metabolism. Investigating the placenta is an opportunity for future research as it may help to understand the fundamental biology underpinning the DOHaD concept through the interactions between the underlying modes of action, prenatal environment, and disease risk in later life. To prevent lasting consequences from early-life exposures of air pollution, policy makers should get a basic understanding of biomolecular consequences and transgenerational risks.

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Differential DNA methylation and PM_2.5 species in a 450K epigenome-wide association study

Cited by 56 publications

References 54 publications

Accelerated DNA methylation age and the use of antihypertensive medication among older adults

Accelerated DNA methylation age and the use of antihypertensive medication among older adults

Differential Association of Mitochondrial DNA Haplogroups J and H With the Methylation Status of Articular Cartilage: Potential Role in Apoptosis and Metabolic and Developmental Processes

Air pollution-induced placental alterations: an interplay of oxidative stress, epigenetics, and the aging phenotype?

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Differential DNA methylation and PM2.5 species in a 450K epigenome-wide association study

Cited by 56 publications

References 54 publications

Accelerated DNA methylation age and the use of antihypertensive medication among older adults

Accelerated DNA methylation age and the use of antihypertensive medication among older adults

Differential Association of Mitochondrial DNA Haplogroups J and H With the Methylation Status of Articular Cartilage: Potential Role in Apoptosis and Metabolic and Developmental Processes

Air pollution-induced placental alterations: an interplay of oxidative stress, epigenetics, and the aging phenotype?

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Differential DNA methylation and PM_2.5 species in a 450K epigenome-wide association study