Epigenetics modifications involved in fetal growth restriction due to maternal smoking during pregnancy
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE218721 | GEO | 2025/01/21
REPOSITORIES: GEO
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Project description:IntroductionSmoking during pregnancy is associated with reduced foetal growth, amongst other effects. Epigenetic modification in the foetus and placenta during embryonic development as a result of changes in the function of miRNAs is one of the pathophysiological mechanisms responsible for this. This dysregulation may be due to environmental changes or toxins such as tobacco.ObjectiveTo study the impact of smoking during pregnancy and its role in intrauterine growth restriction via hypermethylated miRNAs.Materials and methodsThe differences in methylation patterns for miRNAs in umbilical cord blood from low-birth-weight newborns of smoking mothers were compared with those from normal-weight newborns using MedIP-seq (StarArray).ResultsSeven hypermethylated miRNAs were identified in the epigenetic study of cord blood from low-birth-weight newborns of smoking mothers in our sample. The miRNAs found to be hypermethylated were: MIR7-1, MIR3918, MIR1244-1, MIR4721, MIR25, MIR93, MIR3656.ConclusionIntrauterine exposure to tobacco induces hypermethylation-mediated miRNA silencing in low-birth-weight newborns by modifying the expression of factors involved in vascular development, growth, and adaptation to hypoxia.
| S-EPMC9571148 | biostudies-literature
Project description:Background; Intrauterine exposure to maternal smoking is linked to impaired executive function and behavioral problems in the offspring. Maternal smoking is associated with reduced fetal brain growth and smaller volume of cortical grey matter in childhood, indicating that prenatal exposure to tobacco may impact cortical development and manifest as behavioral problems. Cellular development is mediated by changes in epigenetic modifications such as DNA methylation, which can be affected by exposure to tobacco. Results: In this study we sought to ascertain how maternal smoking during pregnancy affects global DNA methylation profiles of the developing dorsolateral prefrontal cortex (DLPFC) during the second trimester of gestation. When DLPFC methylation profiles (Illumina, HM450) of smoking-exposed and unexposed fetuses were compared, no differentially methylated regions (DMRs) passed false discovery correction (FDR ² 0.05). However, the most significant DMRs were hypomethylated CpG Islands within the promoter regions of GNA15 and SDHAP3 of smoking-exposed fetuses. Furthermore, developmental up-regulation of SDHAP3 mRNA was delayed in smoking- exposed fetuses. DMRÕs passing FDR were found by interaction analysis between gestational age and smoking exposure annotated to SYCE3, C21orf56/LSS, SPAG1 and RNU12/POLDIP3. Utilizing established methods to estimate cell proportions by DNA methylation, we found that exposed DLPFC samples contained a lower proportion of neurons in samples from fetuses exposed to maternal smoking. We further showed that nicotine impedes the differentiation of neurons in vitro independent of cell death. Conclusions; We found evidence that intrauterine smoking exposure alters the developmental patterning of DNA methylation and gene expression and is associated with reduced mature neuronal content, effects that are likely driven by nicotine.
2017-02-19 | GSE90871 | GEO
Project description:To investigate the role of smoking in the rupture of intracranial aneurysms (IA), plasma miRNA profiles of smoking IA patients, non-smoking IA patients, and healthy volunteers were analyzed.
2023-11-15 | GSE231922 | GEO
Project description:Transcriptional analysis of placenta samples exposed to maternal smoking during pregnancy
| PRJNA1064129 | ENA
Project description:Genetic Architecture of Smoking and Smoking Cessation
| PRJNA75689 | ENA
Project description:DNA methylation analysis of placenta samples exposed to maternal smoking during pregnancy
| PRJNA717173 | ENA
Project description:Rationale: Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD) and lung cancer remains significantly higher compared to never-smokers. Objectives: Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE), we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. Methods: SAE was collected from 10th to 12th order bronchi using fiberoptic bronchoscopy. Affymetrix miRNA 2.0 arrays were used to assess miRNA expression in the SAE from 10 healthy never-smokers and 10 healthy smokers, before and after they quit for 3 months. Smoking status was determined by urine nicotine and cotinine measurement. Results: There were significant differences in the expression of 34 miRNAs between healthy smokers and healthy never-smokers (p<0.01, fold-change >1.5), with functions associated with lung development, airway epithelium differentiation, inflammation and cancer. After quitting smoking for 3 months, 12 out of the 34 miRNAs did not return to normal levels, with Wnt/β-catenin signaling pathway the top enriched pathway of the target genes of the persistent deregulated miRNAs. Conclusions: In the context that many of these persistent smoking-dependent miRNAs are associated with differentiation, inflammation diseases or lung cancer, it is likely that persistent smoking-related changes in small airway epithelium miRNAs play a role in the subsequent development of these disorders.
2015-11-23 | GSE53519 | GEO
Project description:Maternal smoking during pregnancy has been consistently related to low birthweight. However, older mothers, who are already at risk of giving birth to low birthweight infants, might be even more susceptible to the effects of maternal smoking. Therefore, this study aimed to examine the modified association between maternal smoking and low birthweight by maternal age.Data were obtained from a questionnaire survey of all mothers of children born between 2004 and 2010 in Okinawa, Japan who underwent medical check-ups at age 3 months. Variables assessed were maternal smoking during pregnancy, maternal age, gestational age, parity, birth year, and complications during pregnancy. Stratified analyses were performed using a logistic regression model.In total, 92641 participants provided complete information on all variables. Over the 7 years studied, the proportion of mothers smoking during pregnancy decreased from 10.6% to 5.0%, while the prevalence of low birthweight did not change remarkably (around 10%). Maternal smoking was significantly associated with low birthweight in all age groups. The strength of the association increased with maternal age, both in crude and adjusted models.Consistent with previous studies conducted in Western countries, this study demonstrates that maternal age has a modifying effect on the association between maternal smoking and birthweight. This finding suggests that specific education and health care programs for older smoking mothers are important to improve their foetal growth.
| S-EPMC4721610 | biostudies-other
Project description:BackgroundAn obstetrical paradox is that maternal smoking is protective for the development of preeclampsia. However, there are no prior studies investigating the risk of preeclampsia in women who were exposed to tobacco smoking during their own fetal period. We aimed to study the subsequent risk of preeclampsia in women who were exposed to tobacco smoke in utero, using a national population-based register.MethodsData were obtained from the Medical Birth Register of Sweden for women who were born in 1982 (smoking data first recorded) or after, who had given birth to at least one child; 153 885 pregnancies were included.ResultsThe associations between intrauterine smoking exposure (three categories: non-smokers, 1-9 cigarettes/day [moderate exposure], and >9 cigarettes/day [heavy exposure]) and subsequent preeclampsia (n = 5721) were assessed using logistic regressions. In models adjusted for maternal age, parity and own smoking, the odds ratios (OR) for preeclampsia were 1.06 [95% CI: 0.99,1.13 for moderate intrauterine exposure, and 1.18, [95% CI: 1.10,1.27] for heavy exposure. Estimates were slightly strengthened in non-smoking women who experienced heavy intrauterine exposure (adjusted OR 1.24 [95% CI: 1.14,1.34]). Results were no longer statistically significant after adjustment for the woman's own BMI, gestational age and birthweight Z-scores.ConclusionThese data revealed some evidence of a possible weak positive association between intrauterine smoking exposure and the risk of subsequent preeclampsia, however, results were not significant over all manifestations of preeclampsia and confounder adjustment. The increased risk might be mediated through exposed women's own BMI or birthweight.
| S-EPMC4667973 | biostudies-literature
Project description:Alcohol exposure is known to impact several components of the one-carbon metabolism pathway, which is vital for providing methyl groups for DNA and peptide synthesis and for methylation modification of nucleotides and proteins. Methylation patterning in DNA is known to be altered across generations in specific situations in humans, including nutrient deprivation and smoking during pregnancy. We were interested in seeing whether heavy alcohol exposure during pregnancy, which is associated with fetal alcohol syndrome, influences genome-wide infant methylation patterning. From Guthrie card spots across over 100 infants of various genders, ethnicities, and maternal smoking and drinking status, we find two loci that are have significantly different methylation patterning associated with maternal drinking; cgXXX and cgYYY, the former near MCOLN3 and the latter in intergenic space. We also use available epidemiological information associated with our data set to replicate maternal smoking with infant methylation changes as well as replicate and expand upon methylation differences between genders and ethnicities.
2016-01-29 | GSE65428 | GEO