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Background In the early-life environment, proper development of the placenta is essential for both fetal and maternal health. Telomere length at birth has been related to life expectancy. MicroRNAs (miRNAs) as potential epigenetic determinants of telomere length at birth have not been identified. In this study, we investigate whether placental miRNA expression is associated with placental telomere length at birth. Methods We measured the expression of seven candidate miRNAs (miR-16-5p, -20a-5p, -21-5p, -34a-5p, 146a-5p, -210-3p and -222-3p) in placental tissue at birth in 203 mother-newborn (51.7% girls) pairs from the ENVIR ON AGE birth cohort. We selected miRNAs known to be involved in crucial cellular processes such as inflammation, oxidative stress, cellular senescence related to aging. Placental miRNA expression and relative average placental telomere length were measured using RT-qPCR. Results Both before and after adjustment for potential covariates including newborn’s ethnicity, gestational age, paternal age, maternal smoking status, maternal educational status, parity, date of delivery and outdoor temperature during the 3rd trimester of pregnancy, placental miR-34a, miR-146a, miR-210 and miR-222 expression were significantly ( p  ≤  0.03 ) and positively associated with placental relative telomere length in newborn girls. In newborn boys, only higher expression of placental miR-21 was weakly ( p  =  0.08 ) associated with shorter placental telomere length. Significant miRNAs explain around 6–8% of the telomere length variance at birth. Conclusions Placental miR-21, miR-34a, miR-146a, miR-210 and miR-222 exhibit sex-specific associations with telomere length in placenta. Our results indicate miRNA expression in placental tissue could be an important determinant in the process of aging starting from early life onwards.

Background HIF1α, miR-210 and its downstream targets ISCU, COX-10, RAD52 and PTEN are all part of the placental hypoxia-responsive network. Tight regulation of this network is required to prevent development of maternal–fetal complications such as fetal growth restriction. HIF1α expression is increased in preeclamptic placentae, but little is known about its association with birth weight in normal pregnancies. Methods We measured placental levels of HIF1α , miR-20a, miR-210, ISCU , COX - 10 , RAD52 and PTEN in 206 mother–newborn pairs of the ENVIR ON AGE birth cohort. Results Placental HIF1α gene expression was inversely associated with the ponderal index (PI): for a doubling in placental HIF1α expression, PI decreased by 6.7% (95% confidence interval [CI] 1.3 to 12.0%, p = 0.01). Placental RAD52 expression also displayed an inverse association with PI, a doubling in gene expression was associated with a 6.2% (CI 0.2 to 12.1% p = 0.04) decrease in PI. As for birth weight, we observed a significant association with placental miR-20a expression only in boys, where a doubling in miR-20a expression is associated with a 54.2 g (CI 0.6 to 108 g, p = 0.05) increase in birth weight. Conclusions The decrease in fetal growth associated with expression of hypoxia-network members HIF1a, RAD52 and miR-20a indicates that this network is important in potential intrauterine insults.

There is increasing evidence that the predisposition for development of chronic diseases arises at the earliest times of life. In this context, maternal pre-pregnancy weight might modify fetal metabolism and the child’s predisposition to develop disease later in life. The aim of this study is to investigate the association between maternal pre-pregnancy body mass index (BMI) and miRNA alterations in placental tissue at birth. In 211 mother-newborn pairs from the ENVIR ON AGE birth cohort, we assessed placental expression of seven miRNAs important in crucial cellular processes implicated in adipogenesis and/or obesity. Multiple linear regression models were used to address the associations between pre-pregnancy BMI and placental candidate miRNA expression. Maternal pre-pregnancy BMI averaged (±SD) 23.9 (±4.1) kg/m 2 . In newborn girls (not in boys) placental miR-20a, miR-34a and miR-222 expression was lower with higher maternal pre-pregnancy BMI. In addition, the association between maternal pre-pregnancy BMI and placental expression of these miRNAs in girls was modified by gestational weight gain. The lower expression of these miRNAs in placenta in association with pre-pregnancy BMI, was only evident in mothers with low weight gain (<14 kg). The placental expression of miR-20a, miR-34a, miR-146a, miR-210 and miR-222 may provide a sex-specific basis for epigenetic effects of pre-pregnancy BMI.

Background Due to their lack of repair capacity mitochondria are critical targets for environmental toxicants. We studied genes and pathways reflecting mitochondrial responses to short- and medium-term PM 10 exposure. Methods Whole genome gene expression was measured in peripheral blood of 98 adults (49% women). We performed linear regression analyses stratified by sex and adjusted for individual and temporal characteristics to investigate alterations in gene expression induced by short-term (week before blood sampling) and medium-term (month before blood sampling) PM 10 exposure. Overrepresentation analyses (ConsensusPathDB) were performed to identify enriched mitochondrial associated pathways and gene ontology sets. Thirteen Human MitoCarta genes were measured by means of quantitative real-time polymerase chain reaction (qPCR) along with mitochondrial DNA (mtDNA) content in an independent validation cohort ( n  = 169, 55.6% women). Results Overrepresentation analyses revealed significant pathways ( p -value <0.05) related to mitochondrial genome maintenance and apoptosis for short-term exposure and to the electron transport chain (ETC) for medium-term exposure in women. For men, medium-term PM 10 exposure was associated with the Tri Carbonic Acid cycle. In an independent study population, we validated several ETC genes, including UQCRH and COX7C ( q -value <0.05), and some genes crucial for the maintenance of the mitochondrial genome, including LONP1 ( q -value: 0.07) and POLG ( q -value: 0.04) in women. Conclusions In this exploratory study, we identified mitochondrial genes and pathways associated with particulate air pollution indicating upregulation of energy producing pathways as a potential mechanism to compensate for PM-induced mitochondrial damage.

Background Air pollution exposure during pregnancy has been associated with adverse birth outcomes and health problems later in life. We investigated sex-specific transcriptomic responses to gestational long- and short-term exposure to particulate matter with a diameter < 2.5 μm (PM 2.5 ) in order to elucidate potential underlying mechanisms of action. Methods Whole genome gene expression was investigated in cord blood of 142 mother-newborn pairs that were enrolled in the ENVIR ON AGE birth cohort. Daily PM 2.5 exposure levels were calculated for each mother’s home address using a spatial-temporal interpolation model in combination with a dispersion model to estimate both long- (annual average before delivery) and short- (last month of pregnancy) term exposure. We explored the association between gene expression levels and PM 2.5 exposure, and identified modulated pathways by overrepresentation analysis and gene set enrichment analysis. Results Some processes were altered in both sexes for long- (e.g. DNA damage) or short-term exposure (e.g. olfactory signaling). For long-term exposure in boys neurodevelopment and RhoA pathways were modulated, while in girls defensin expression was down-regulated. For short-term exposure we identified pathways related to synaptic transmission and mitochondrial function (boys) and immune response (girls). Conclusions This is the first whole genome gene expression study in cord blood to identify sex-specific pathways altered by PM 2.5 . The identified transcriptome pathways could provide new molecular insights as to the interaction pattern of early life PM 2.5 exposure with the biological development of the fetus.

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and fibromyalgia (FM) are chronic syndromes of unknown etiology, accompanied by numerous symptoms affecting neurological and physical conditions. Despite frequent revisions of the diagnostic criteria, clinical practice guidelines are often outdated, leading to underdiagnosis and ineffective treatment. Our aim was to identify microRNA (miRNA) biomarkers implicated in pathological mechanisms underlying these diseases. A comprehensive literature review using publicly accessible databases was conducted. Interesting miRNAs were extracted from relevant publications on ME/CFS and/or FM, and were then linked to pathophysiological processes possibly manifesting these chronic diseases. Dysregulated miRNAs in ME/CFS and FM may serve as promising biomarkers for these diseases. Key identified miRNAs, such as miR-29c, miR-99b, miR-128, miR-374b, and miR-766, were frequently mentioned for their roles in immune response, mitochondrial dysfunction, oxidative stress, and central sensitization, while miR-23a, miR-103, miR-152, and miR-320 were implicated in multiple crucial pathological processes for FM and/or ME/CFS. In summary, both ME/CFS and FM seem to share many dysregulated biological or molecular processes, which may contribute to their commonly shared symptoms. This miRNA-based approach offers new angles for discovering molecular markers urgently needed for early diagnosis or therapeutics to tackle the pathology of these medically unexplained chronic diseases.

Particulate matter (PM) exposure leads to premature death, mainly due to respiratory and cardiovascular diseases. Identification of transcriptomic biomarkers of air pollution exposure and effect in a healthy adult population. Microarray analyses were performed in 98 healthy volunteers (48 men, 50 women). The expression of eight sex-specific candidate biomarker genes (significantly associated with PM in the discovery cohort and with a reported link to air pollution-related disease) was measured with qPCR in an independent validation cohort (75 men, 94 women). Pathway analysis was performed using Gene Set Enrichment Analysis. Average daily PM and PM exposures over 2-years were estimated for each participant's residential address using spatiotemporal interpolation in combination with a dispersion model. Average long-term PM was 25.9 (± 5.4) and 23.7 (± 2.3) μg/m in the discovery and validation cohorts, respectively. In discovery analysis, associations between PM and the expression of individual genes differed by sex. In the validation cohort, long-term PM was associated with the expression of and in men and ( = 0.053) in women. and were significantly associated with PM in women, although associations differed in direction between the discovery and validation cohorts. Expression of the eight candidate genes in the discovery cohort differentiated between validation cohort participants with high versus low PM exposure (area under the receiver operating curve = 0.92; 95% CI: 0.85, 1.00; = 0.0002 in men, 0.86; 95% CI: 0.76, 0.96; = 0.004 in women). Expression of the sex-specific candidate genes identified in the discovery population predicted PM exposure in an independent cohort of adults from the same area. Confirmation in other populations may further support this as a new approach for exposure assessment, and may contribute to the discovery of molecular mechanisms for PM-induced health effects.

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Epidemiological studies in adults have linked air pollution's adverse effects to alterations in gene expression profiles, which can be regulated by epigenetic mechanisms, including microRNAs (miRNAs). Volume 73 Supplement 1 Methods in Epidemiology Symposium [RAW_REF_TEXT] Poster presentation [/RAW_REF_TEXT] [RAW_REF_TEXT] Open Access [/RAW_REF_TEXT] [RAW_REF_TEXT] Published:17 September 2015 [/RAW_REF_TEXT] Placental miRNA expression in association with in utero particulate air pollution exposure [RAW_REF_TEXT] Maria Tsamou 1 , [/RAW_REF_TEXT] [RAW_REF_TEXT] Karen Vrijens1 , [/RAW_REF_TEXT] [RAW_REF_TEXT] Narjes Madhloum1 , [/RAW_REF_TEXT] [RAW_REF_TEXT] Wouter Lefebvre2 , [/RAW_REF_TEXT] [RAW_REF_TEXT] Charlotte Vanpoucke3 , [/RAW_REF_TEXT] [RAW_REF_TEXT] Wilfried Gyselaers4 & [/RAW_REF_TEXT] [RAW_REF_TEXT] Tim S Nawrot1 [/RAW_REF_TEXT] Archives of Public Health volume 73, Article number: P36 (2015) Cite this article [RAW_REF_TEXT] 484 Accesses [/RAW_REF_TEXT] [RAW_REF_TEXT] 1 Citations [/RAW_REF_TEXT] [RAW_REF_TEXT] Metrics details [/RAW_REF_TEXT] Poster presentation Open Access Published:17 September 2015 [/RAW_REF_TEXT] Placental miRNA expression in association with in utero particulate air pollution exposure [RAW_REF_TEXT] Maria Tsamou 1 , Karen Vrijens1 , Narjes Madhloum1 , Wouter Lefebvre2 , Charlotte Vanpoucke3 , Wilfried Gyselaers4 & Tim S Nawrot1 [/RAW_REF_TEXT] Archives of Public Health volume 73, Article number: