Effects of gestational exposure to air pollution on placental methylation mark
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE221069 | GEO | 2025/12/01
REPOSITORIES: GEO
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Project description:We report the distribution of 5-Hydroxymethylation mark by Next Generation Sequencing from Gestational D19 mouse exposed to Air -Pollutant material with or without prior treatment with Fish Oil.
2025-12-01 | GSE221014 | GEO
Project description:We report the expression pattern of placental transcriptome by Next Generation Sequencing from Gestational D19 mouse exposed to Air -Pollutant material with or without prior treatment with Fish Oil.
2022-05-25 | GSE178098 | GEO
Project description:We are reporting the expression pattern of placental transcriptome in a celltype specific manner from Gestational D19 mouse exposed to Air -Pollutant material.
2022-05-25 | GSE178229 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2025-12-01 | GSE221071 | GEO
Project description:Effects of gestational exposure to air pollution on placental transcriptome
| PRJNA737359 | ENA
Project description:Gestational exposure to air pollution increases the risk of autism spectrum disorder and cognitive impairments with unresolved molecular mechanisms. This study exposed mice throughout gestation to urban derived nanosized particulate matter (nPM). Young adult male and female offspring were studied for behavioral and metabolic changes using forced swim test, fat gain, glucose tolerance, and hippocampal transcriptome. Gestational nPM exposure caused increased depressive behaviors, decreased neurogenesis in the dentate gyrus, and increased glucose tolerance in adult male offspring. Both sexes gained fat and body weight. Gestational nPM exposure induced 29 differentially expressed genes (DEGs) in adult hippocampus related to cytokine production, IL17a signaling, and dopamine degradation in both sexes. Stratification by sex showed 2-fold more DEGs in males than females (69 vs 37), as well as male-specific enrichment of DEGs mediating serotonin signaling, endocytosis, Gai, and cAMP signaling. Gene co-expression analysis (WCGNA) identified a module of 43 genes with divergent responses to nPM between the sexes. Chronic changes in 14 DEGs (e.g., miR9-1) were associated with depressive behaviors, adiposity and glucose intolerance. These genes enriched neuroimmune pathways such as HMGB1 and TLR4. Based on cerebral cortex transcriptome data of neonates, we traced the initial nPM responses of HMGB1 pathway. In vitro, mixed glia responded to 24 h nPM with lower HMGB1 protein and increased proinflammatory cytokines. This response was ameliorated by TLR4 knockdown. In sum, we identified transcriptional changes that could underlie air pollution mediated behavioral and phenotypic changes. These identified genes merit further studies for therapeutic intervention development.
2020-07-07 | GSE147842 | GEO
Project description:Restricted fetal growth (RFG) is a leading contributor to perinatal mortality and has been associated with gestational exposure to air pollution, such as fine particulate matter (PM2.5), nitrogen dioxide (NO2), and polycyclic aromatic hydrocarbons (PAHs). This study examines the association between trimester-specific and weekly means of air pollution throughout gestation and placental inflammatory markers at delivery. In a prospective cohort study of 263 pregnant women in Rochester, NY, we measured interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) in placental tissue and estimated gestational exposure to PM2.5 and NO2 using a high-resolution spatial-temporal model. Exposure to PAHs was estimated using urinary 1-hydroxypyrene (1-OHP) concentrations collected once per trimester. Using distributed lag models with a penalized spline function, each interquartile range (2.6 μg/m3) increase in PM2.5 concentration during gestational weeks 6-11 was associated with decreased placental IL-6 levels (-22.2%, 95% CI: -39.0%, -0.64%). Using multiple linear regression models, each interquartile range increase of 1-OHP was associated with an increase in TNF-α in the first trimester (58.5%, 95% CI: 20.7%, 74.2%), third trimester (22.9%, 95% CI: 0.04%, 49.5%), and entire pregnancy (29.6%, 95%CI: 3.9%,60.6%). Our results suggest gestational exposure to air pollution may alter the inflammatory environment of the placenta at delivery.
| S-EPMC11420950 | biostudies-literature
Project description:Background: Gestational age determination by traditional tools (last menstrual period, ultrasonography measurements and Ballard Maturational Assessment in newborns) have major limitations and therefore there is a need to find molecular marker approaches that can be used to determine the accurate gestational age of the newborn. Methods: We performed RRBS (Reduced Representation Bisulfite Sequencing) on 41 cord blood and matching placenta samples. Results: We identified a set of 316 Differentially Methylated Regions (DMRs) that undergo demethylation in late gestational age in cord blood cells and can predict the gestational age (r = -0.7, p value<0.0001). Once the set of 411 DMRs that undergo de novo methylation in late gestational age was used in combination with the first set it generated a more accurate clock (r=0.77, p value=1.87E-05). Conclusion: Taken together, this study demonstrates that DNA methylation can accurately predict gestational age. The clinical use of this predictor should be further investigated.
2019-07-18 | GSE109538 | GEO
Project description:Introduction: Air pollution is detrimental to a pregnancy with adverse effects in mother and child. It is also known to increase pregnancy complications including risk factors of gestational diabetes. Methods: We investigated the impact of intra-nasal instilled air pollutants upon gestational day 16-19 maternal mouse cardiovascular and metabolic status, placental nutrient transporters, and placental-fetal size and morphology. To further unravel mechanisms, we also examined placental total DNA 5’-hydroxymethylation and bulk RNA sequenced gene expression profiles. Results: Air pollution exposed pregnant mice were tachycardic, hyperglycemic, glucose intolerant and insulin resistant, with no major placental glucose and fatty acid transporter changes, except for a spatial disruption of cells expressing GLUT10 that imports L-dehydroascorbic acid in protecting against oxidative stress. Placentas revealed inflammatory cellular infiltration with associated cellular edema and necrosis, with a paucity of vascularity and hemorrhage. While individual fetal body weights increased, they suffered a reduction in brain cortical thickness. Placental total DNA 5’-hydroxymethylation was 2.5-fold higher, with perturbed gene expression profiles involving key metabolic, inflammatory, transcriptional, cellular polarizing and processing genes and pathways. Discussion: We conclude that gestational exposure to air pollutants incites a maternal inflammatory response resulting in features of maternal gestational diabetes mellitus with altered placental gene expression with associated injury to the placental-fetal unit. Thus, air pollutants adversely impact the health of mother and offspring.
2025-03-07 | GSE261095 | GEO
Project description:Air pollution has been linked to hypertension in the general population, but data on gestational hypertension (GH) are limited. We investigated criteria air pollutants and air toxics during the period before conception and in early gestation in relation to GH risk in the Consortium on Safe Labor/Air Quality and Reproductive Health Study (United States, 2002-2008). Modified Community Multi-scale Air Quality models estimated air pollution exposures for 6,074 singleton pregnancies in which GH was present and 199,980 normotensive pregnancies. Generalized estimating equations estimated relative risks per interquartile-range increment for pollutants and high exposure (≥75th percentile) for air toxics after adjustment for major risk factors. For an interquartile-range increment, GH risk was significantly increased by 18% for sulfur dioxide during the 3 months before conception and, during gestational weeks 1-20, 17% for nitrogen oxides, 10% for particulate matter with an aerodynamic diameter <2.5 μm, 7% for particulate matter with an aerodynamic diameter <10 μm, and 22% for sulfur dioxide. High exposures to several polycyclic aromatic hydrocarbons before conception and during the first trimester were significantly associated with 8%-20% higher risk of GH. Further, preconceptional exposures to several volatile organic compounds were significantly associated with 11%-19% higher risk. Our findings suggest that early exposures to criteria air pollutants, particularly from transport emissions, and high exposure to several air toxics before conception may increase GH risk.
| S-EPMC5860464 | biostudies-literature