Placental mRNA Expression data from pregnant smokers and non-smokers
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE71931 | GEO | 2016/08/08
SECONDARY ACCESSION(S): PRJNA292496
REPOSITORIES: GEO
Similar Datasets
Project description:We used microarrays to determine the transcriptional profiles of placental tissue obtained from women who smoked during pregnancy and from women who did not smoke during pregnancy. Fetal growth restriction is a frequent complication in mothers who smoke cigarettes during pregnancy. To evaluate novel pathways that regulate fetal growth affected by mothers who smoke, we isolated placental mRNA from smoking mothers with severe fetal growth restriction and compared them by microarray analysis to non-smoking mothers with appropriately grown fetuses. Bioinformatics analysis revealed distinct transcriptional patterns in the placentas of smoking mothers when compared to placentas from control non-smoking women. Analyses of the top upregulated and downregulated genes revealed several gene products such as secreted frizzled related protein 1 that was markedly upregulated in the placentas from women who smoked cigarettes during pregnancy. Total RNA was isolated from placental specimens obtained at time of delivery. RNA was hybridized to Affymetrix arrays, and analyzed.
2016-08-08 | E-GEOD-71931 | biostudies-arrayexpress
Project description:Passive smoke intake by pregnant women may have detrimental effects such as spontaneous abortion, lower birth weight, stillbirth, and reduced infant lung function. To extend our knowledge on molecular effects of tobacco smoke exposure in pregnancy, we analyzed transcriptome alterations in passive smokers (PS) and compared them to those in active smokers (AS). Using Illumina Expression Beadchip with 24,526 transcript probes, gene expression patterns were assayed in placentas from PS (N=25) exposed to environmental tobacco smoke (ETS) throughout pregnancy and non-exposed (NS) counterparts (N=35), and in cord blood cells from their newborns. The ETS exposure was evaluated by questionnaire disclosure and cotinine measurement in maternal and cord bloods. A total of 196 genes were significantly deregulated in placentas of PS compared to NS. These genes were primary associated with extracellular matrix, apoptosis, blood clotting, response to stress, embryonic morphogenesis, and lipid metabolism. Cord blood of newborns of PS displayed differential expression of 116 genes encoding mainly neuronal factors, regulators of immunologic response, and protooncogenes. Gene ontology analyses highlighted some important biological processes that might be associated with placental insufficiency and fetal growth restriction in PS, such as fatty acid catabolism, coagulation, regulation of growth, and response to steroid hormone stimulus. The study demonstrates that even low dose exposure to ETS during pregnancy leads to the significant deregulation of transcriptional regulation in placental and fetal cells. The data suggest the effect of ETS on the fetus is primary indirect, mediated via deregulation of placental functions. Comparison of PS and AS indicated that ETS exposure and active smoking in pregnancy partly employ the same molecular mechanisms. A total of 60 women who gave birth to a baby in the Faculty Hospital Motol (Czech Republic) were enrolled into the study approved by the local Institutional Review Board. The participants signed written informed consent and self-reported information on tobacco smoke exposure (type of exposure, number of cigarettes per day, exposure period) and life style during pregnancy (alcohol drinking, diet, area of residency etc.). Further, the women completed the questionnaire on pregnancy/delivery course (complications, diseases, medication, and delivery mode) and newborn characteristics (physical parameters, Apgar score) with the assistance of gynecologist. Only women without any health complications during pregnancy and their newborns without manifestation of pathological abnormalities were included in the study. Based on self-reported tobacco smoke exposure, the women were divided into two groups, non-smokers (NS, N=35) and passive smokers (PS, N=25). Former and active smokers were excluded from the study. Exposure to tobacco smoke was further evaluated by measurement of plasma cotinine levels in maternal peripheral blood and newborn cord blood using radioimmunoassay.
2011-07-19 | E-GEOD-30032 | biostudies-arrayexpress
Project description:Maternal smoking has a severe negative effect on all stages of pregnancy that in consequence impairs fetal growth and development. Tobacco smoke-related defects are well established at the clinical level; however, little is known about molecular mechanisms underlying these pathological conditions. We thus employed a genomic approach to determine transcriptome alterations induced by maternal smoking in pregnancy. We assayed gene expression profiles in peripheral blood (M) leukocytes and placentas (PL) of pregnant smokers and those without significant exposure, and in cord blood (D) leukocytes of their babies. Comparative analyses defined significant deregulation of 193 genes in M cells, 329 genes in placentas, and 49 genes in D cells of smokers. These genes were mainly involved in xenobiotic metabolism, oxidative stress, inflammation, immunity, hematopoiesis, trophoblast differentiation, and vascularization. Functional annotation of the deregulated genes outlined processes and pathways affected by tobacco smoke. In smoker newborns, we identified several deregulated pathways associated with autoimmune diseases. The study demonstrates a limited ability of placenta to modulate toxic effects of maternal tobacco use at the gene expression level. Blood and placental samples were obtained from 91 women who gave birth to a baby in the Ceske Budejovice Hospital from November 2008 to March 2009. The study was approved by the Local Institutional Review Board. All participants provided written informed consent and completed an extensive questionnaire on pregnancy history (medication, diseases), delivery course, newborn characteristics and life style (smoking, diet, alcohol drinking, area of residency). Only subjects who underwent vaginal delivery were included in the study. Based on smoking history, the women were divided into two groups, “smokers” (N=20) and “non-smokers” (N=52), while passive smokers (N=19) were excluded from the study. Smoking status was further confirmed by detection of excessive plasma levels of cotinine (the major nicotine metabolite) in maternal blood.
2011-04-01 | E-GEOD-27272 | biostudies-arrayexpress
Project description:Smoking in pregnancy increases a woman's risk of preterm delivery resulting in serious health problems during the newborn period, chronic lifelong disabilities (such as cerebral palsy, mental retardation and learning problems), and even death. Further, smoking women have placental problems such as placenta previa (a low-lying placenta that covers part or all of the opening of the uterus), placental abruption (in which the placenta peels away, partially or almost completely before delivery) often resulting in bleeding during delivery. Gene expression profiles in placentas from women exposed to tobacco smoke in pregnancy and from those without the exposure were determined by Illumina HumRef8 Beadchips with 20,589 gene probes. Comparative analysis, smokers versus non-smokers, revealed differential expression of 241 genes at p<0.05. In smokers we identified deregulated genes that represent general biomarkers of exposure as well as candidate genes likely involved in placental abnormalities found in smoking women. Functional annotation determined deregulated processes that were mainly related to development, metabolism, ion transport, and adhesion.
2009-09-15 | GSE18044 | GEO
Project description:Gene expression in placenta from 5 smoking and 5 non-smoking mothers analyzed by Affymetrix Hg133_plus2 microarrays. Keywords: Toxic response
2007-10-01 | GSE7434 | GEO
Project description:Maternal smoking has a severe negative effect on all stages of pregnancy that in consequence impairs fetal growth and development. Tobacco smoke-related defects are well established at the clinical level; however, little is known about molecular mechanisms underlying these pathological conditions. We thus employed a genomic approach to determine transcriptome alterations induced by maternal smoking in pregnancy. We assayed gene expression profiles in peripheral blood (M) leukocytes and placentas (PL) of pregnant smokers and those without significant exposure, and in cord blood (D) leukocytes of their babies. Comparative analyses defined significant deregulation of 193 genes in M cells, 329 genes in placentas, and 49 genes in D cells of smokers. These genes were mainly involved in xenobiotic metabolism, oxidative stress, inflammation, immunity, hematopoiesis, trophoblast differentiation, and vascularization. Functional annotation of the deregulated genes outlined processes and pathways affected by tobacco smoke. In smoker newborns, we identified several deregulated pathways associated with autoimmune diseases. The study demonstrates a limited ability of placenta to modulate toxic effects of maternal tobacco use at the gene expression level.
2011-04-01 | GSE27272 | GEO
Project description:Passive smoke intake by pregnant women may have detrimental effects such as spontaneous abortion, lower birth weight, stillbirth, and reduced infant lung function. To extend our knowledge on molecular effects of tobacco smoke exposure in pregnancy, we analyzed transcriptome alterations in passive smokers (PS) and compared them to those in active smokers (AS). Using Illumina Expression Beadchip with 24,526 transcript probes, gene expression patterns were assayed in placentas from PS (N=25) exposed to environmental tobacco smoke (ETS) throughout pregnancy and non-exposed (NS) counterparts (N=35), and in cord blood cells from their newborns. The ETS exposure was evaluated by questionnaire disclosure and cotinine measurement in maternal and cord bloods. A total of 196 genes were significantly deregulated in placentas of PS compared to NS. These genes were primary associated with extracellular matrix, apoptosis, blood clotting, response to stress, embryonic morphogenesis, and lipid metabolism. Cord blood of newborns of PS displayed differential expression of 116 genes encoding mainly neuronal factors, regulators of immunologic response, and protooncogenes. Gene ontology analyses highlighted some important biological processes that might be associated with placental insufficiency and fetal growth restriction in PS, such as fatty acid catabolism, coagulation, regulation of growth, and response to steroid hormone stimulus. The study demonstrates that even low dose exposure to ETS during pregnancy leads to the significant deregulation of transcriptional regulation in placental and fetal cells. The data suggest the effect of ETS on the fetus is primary indirect, mediated via deregulation of placental functions. Comparison of PS and AS indicated that ETS exposure and active smoking in pregnancy partly employ the same molecular mechanisms.
2011-07-20 | GSE30032 | GEO
Project description:Gene expression in placenta from 5 smoking and 5 non-smoking mothers analyzed by Affymetrix Hg133_plus2 microarrays. Experiment Overall Design: Gene expression in placenta from 5 smoking and 5 non-smoking mothers analyzed by Affymetrix Hg133_plus2 microarrays.
2008-06-15 | E-GEOD-7434 | biostudies-arrayexpress
Project description:We analyzed total leukocyte gene expression using Affymetrix microarrays from healthy smokers, COPD patients and non-smoking control subjects before and after exposure to acute cigarette smoke (smoking two cigarettes in 30 minutes).
2014-07-02 | GSE55962 | GEO
Project description:Cigarette smoke is a major risk factor for the development and progression of chronic obstructive pulmonary disease. Tobacco smoking is also the main cause of lung cancer and the main preventable cause of other lung and heart disease. Strategies to eliminate cigarette smoking have led to the emergence of new tobacco-related products as alternatives for cigarette smoking or tools for smoking cessation. Electronic cigarettes (E-cigarettes) have been introduced to the market in recent years as an alternative to smoking conventional cigarettes. E-cigarettes are nicotine delivery devices by heating and converting to aerosol a liquid mixture composed of propylene glycol, vegetable glycerine, flavouring chemicals, and nicotine. Despite the lack of appropriate studies, e-cigarettes are nowadays widely used and advertised as safe cigarette replacements and the number of users is rapidly growing. Unlike cigarette smoke, where the determinant effects are well studied and documented, very limited amount of research has been done on the health effects and public health of e-cigarettes. The study aims to investigate the effects of e-cigarette vapour extract on gene expression in different primary isolated mouse lung cells [pulmonary arterial smooth muscle cells (PASMC) and alveolar epithelial type two cells (AECII)]. The cells will be exposed to e-cigarette vapour extract (ECVE).
2023-05-01 | GSE202215 | GEO