Transcription profiling of human full-term placenta from smokers and non-smokers
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Markus Storvik
PROVIDER: E-GEOD-7434 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
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: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.
2016-08-08 | GSE71931 | GEO
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:STOX1A overexpression in mice placenta triggers a preeclamptic phenotype in the mothers, with hypertension, proteinuria and kidney alterations (Doridot et al, Hypertension, 2013), this being connected with NO depletion and increase of nutrosative stress (Doridot et al, Antiox Redox Signal, 2014). Tetrahydrobiopterin (BH4) is a cofactor essential for NO production. We treated preeclamptic mice with this drug, and analyzed placental gene expression in four groups (Control mice, Control mice with BH4, Preeclamptic mice and preeclamptic mice with BH4).
2021-05-01 | E-MTAB-9314 | biostudies-arrayexpress
Project description:The initial site of smoking-induced lung disease is the small airway epithelium, which is difficult and time consuming to sample by fiberoptic bronchoscopy. We developed a rapid, office-based procedure to obtain trachea epithelium without conscious sedation from healthy nonsmokers (n=26) and healthy smokers (n=19, 27 ± 15 pack-yr). Gene expression differences [fold-change >1.5, p< 0.01, Benjamini-Hochberg correction] were assessed with Affymetrix microarrays. 1,057 probe sets were differentially expressed in healthy smokers vs nonsmokers, representing >500 genes. Trachea gene expression was compared to an independent group of small airway epithelial samples (n=23 healthy nonsmokers, n=19 healthy smokers, 25 ± 12 pack-yr). The trachea epithelium is more sensitive to smoking, responding with 3-fold more differentially-expressed genes than small airway epithelium. The trachea transcriptome paralleled the small airway epithelium, with 156 of 167 (93%) genes that are significantly up- and down-regulated by smoking in the small airway epithelium showing similar direction and magnitude of response to smoking in the trachea. Trachea epithelium can be obtained without conscious sedation, representing a less invasive surrogate “canary” for smoking-induced changes in the small airway epithelium. This should prove useful in epidemiologic studies correlating gene expression with clinical outcome in assessing smoking-induced lung disease. Experiment Overall Design: Tracheal gene expression: matched group of small airway epithelial samples (n=23 healthy non-smokers, n= 19 healthy smokers)
2009-09-04 | E-GEOD-13933 | biostudies-arrayexpress
Project description:We used full genome microarrays to profile the full lifetime of the mouse placenta from embryonic day 8.5 (e8.5), at the time of chorioallantoic fusion, until postnatal day 0 (P0). For these samples, at each stage the fetal placenta and maternal decidual tissues were dissected and profiled separately (See series 1). For this experiment (Series 2), placental and decidual timecourse samples were normalized and modeled with two undissected (including placental and decidual tissue) e17 placentas to allow for scaling of values for comparison to the undissected placenta samples used in the publicly available mouse GeneAtlas dataset Experiment Overall Design: Mouse placentas were obtained from timed pregnant female mice at each timepoint, and fetal tissues were used to confirm embryo staging. For all dissected samples, fetal placenta and maternal decidual tissues were dissected and pooled separately for each litter prior to RNA extraction and hybridization on Affymetrix microarrays.
2008-06-11 | E-GEOD-11222 | biostudies-arrayexpress
Project description:We used full genome microarrays to profile the full lifetime of the mouse placenta from embryonic day 8.5 (e8.5), at the time of chorioallantoic fusion, until postnatal day 0 (P0). At each stage, the fetal placenta and maternal decidual tissues were dissected and profiled separately Experiment Overall Design: Mouse placentas were obtained from timed pregnant female mice at each timepoint, and fetal tissues were used to confirm embryo staging. Fetal placenta and maternal decidual tissues were dissected and pooled separately for each litter prior to RNA extraction and hybridization on Affymetrix microarrays.
2008-06-11 | E-GEOD-11220 | biostudies-arrayexpress
Project description:An important question for the use of the mouse as a model for studying human disease is the degree of functional conservation of genetic control pathways from human to mouse. The human placenta and mouse placenta show structural similarities but there has been no systematic attempt to assess their molecular similarities or differences. We built a comprehensive database of protein and microarray data for the highly vascular exchange region micro-dissected from the human and mouse placenta near-term. Abnormalities in this region are associated with two of the most common and serious complications of human pregnancy, maternal preeclampsia (PE) and fetal intrauterine growth restriction (IUGR), each disorder affecting ~5% of all pregnancies. To compare the gene expression patterns in the vascular exchange regions of the human (villus tree) and mouse (labyrinth) placenta. Experiment Overall Design: Mouse labyrinth tissue was micro-dissected form naturally mated crosses of C57Bl/6J mice. Placentas were individually dissected on embryonic day 17.5. From each litter ¼ of the tissue were set aside for RNA extraction and microarray analysis and ¾ for cellular fractionation and proteomic analysis, as recently described (Kislinger et al., 2006). Human villous trees were dissected from term normal placenta delivered by cesarean section from a term pregnancy (~ 38 weeks). Tissue was divided for organellar fractionation and RNA extraction.
2009-06-22 | E-GEOD-13155 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series:; GSE11220: Timecourse of developing mouse placenta, with placental and decidual tissues profiled separately; GSE11222: Placental and decidual timecourse samples normalized and modeled with an undissected e17 sample Experiment Overall Design: Refer to individual Series
2008-06-12 | E-GEOD-11224 | biostudies-arrayexpress
Project description:Cigarette smoking is the leading cause of the respiratory diseases collectively known as chronic obstructive pulmonary disease (COPD). While the pathogenesis of COPD is complex, there is abundant evidence that alveolar macrophages (AM) play an important role. Based on the concept that COPD is a slow-progressing disorder likely involving multiple mediators released by AM activated by cigarette smoke, the present study focuses on the identification of previously unrecognized genes that may be linked to early events in the molecular pathogenesis of COPD, as opposed to factors associated with the presence of disease. To accomplish this, microarray analysis using Affymetrix microarrays was used to carry out an unbiased survey of the differences in gene expression profiles in the AM of phenotypically normal, ~20 pack-yr smokers compared to healthy non-smokers. Although smoking did not alter the global gene expression pattern of AM, 75 genes were modulated by smoking, with 40 genes up-regulated and 35 down-regulated in the AM of smokers compared to non-smokers. Most of these genes belong to the functional categories of immune/inflammatory response, cell adhesion and extracellular matrix, proteolysis and antiproteolysis, lysosomal function, antioxidant-related, signal transduction and regulation of transcription. Of these 75 genes, 69 have not been previously recognized to be up- or down-regulated in alveolar macrophages in association with smoking or COPD, including genes coding for proteins belonging to all of the above categories, and others belonging to various functional categories or of unknown function. These observations suggest that gene expression responses of alveolar macrophages associated with the stress of cigarette smoking are more complex than previously thought, and offer a variety of new insights into the complex pathogenesis of smoking-induced lung diseases. Keywords: Comparison of gene expression profile in smokers vs non-smokers
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