Search results for "Placenta"

showing 10 items of 153 documents

Genome-wide DNA methylation study in human placenta identifies novel loci associated with maternal smoking during pregnancy

2016

BACKGROUND: We conducted an epigenome-wide association study (EWAS) of DNA methylation in placenta in relation to maternal tobacco smoking during pregnancy and examined whether smoking-induced changes lead to low birthweight. METHODS: DNA methylation in placenta was measured using the Illumina HumanMethylation450 BeadChip in 179 participants from the INfancia y Medio Ambiente (INMA) birth cohort. Methylation levels across 431 311 CpGs were tested for differential methylation between smokers and non-smokers in pregnancy. We took forward three top-ranking loci for further validation and replication by bisulfite pyrosequencing using data of 248 additional participants of the INMA cohort. We ex…

0301 basic medicineAdultMaleplacentaEpidemiologyMaternal smokingPlacentaEpigenesis GeneticCohort Studies03 medical and health sciencesPregnancyTobacco SmokingMedicineBirth WeightHumansFetal programmingtobacco smokingCotinineDones embarassades -- Consum de tabacDNA methylationepigeneticsbusiness.industryInfant NewbornHuman placentaGeneral MedicineDNA MethylationMendelian Randomization Analysis030104 developmental biologyfetal programmingbirthweightMaternal ExposureSpainLinear ModelsChristian ministryCpG IslandsFemaleDNA -- MetilacióbusinessHumanitiesGenome-Wide Association Study
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Severe pre-eclampsia is associated with alterations in cytotrophoblasts of the smooth chorion.

2016

Pre-eclampsia (PE), which affects ∼8% of first pregnancies, is associated with faulty placentation. Extravillous cytotrophoblasts (CTBs) fail to differentiate properly, contributing to shallow uterine invasion and deficient spiral artery remodeling. We studied the effects of severe PE (sPE) on the smooth chorion portion of the fetal membranes. The results showed a significant expansion of the CTB layer. The cells displayed enhanced expression of stage-specific antigens that extravillous CTBs normally upregulate as they exit the placenta. Transcriptomics revealed the dysregulated expression of many genes (e.g. placental proteins, markers of oxidative stress). We confirmed an sPE-related incr…

0301 basic medicineAdultSpiral arteryTranscription GeneticPlacentaHuman DevelopmentCTBSExtraembryonic MembranesBiology210Andrology03 medical and health sciences0302 clinical medicineDownregulation and upregulationPre-EclampsiaPregnancyPlacentamedicineHumansPregnancy-Associated Plasma Protein-AMolecular BiologyCytotrophoblastPAPPA1Cell ProliferationFetus030219 obstetrics & reproductive medicineCytotrophoblastPlacentationGene Expression Regulation DevelopmentalPreterm birthChorionPlacentationTrophoblastsOxidative Stress030104 developmental biologymedicine.anatomical_structureImmunologyembryonic structuresKeratinsFemaleCytotrophoblastsTranscriptomeDevelopmental BiologyProtein BindingHumanDevelopment (Cambridge, England)
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Characterization of NO-Induced Nitrosative Status in Human Placenta from Pregnant Women with Gestational Diabetes Mellitus

2017

Dysregulation of NO production is implicated in pregnancy-related diseases, including gestational diabetes mellitus (GDM). The role of NO and its placental targets in GDM pregnancies has yet to be determined. S-Nitrosylation is the NO-derived posttranslational protein modification that can modulate biological functions by forming NO-derived complexes with longer half-life, termed S-nitrosothiol (SNO). Our aim was to examine the presence of endogenous S-nitrosylated proteins in cysteine residues in relation to antioxidant defense, apoptosis, and cellular signal transduction in placental tissue from control (n=8) and GDM (n=8) pregnancies. S-Nitrosylation was measured using the biotin-switch …

0301 basic medicineAgingendocrine system diseasesPlacentaNitric Oxide Synthase Type IIExpressionApoptosisBiochemistryBody Mass Index0302 clinical medicineNitric-oxidePregnancyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyCaspase 3lcsh:CytologyNitrosylationP38General MedicineCatalaseCaspase 9TrophoblastsGestational diabetesmedicine.anatomical_structureCatalase030220 oncology & carcinogenesisFemaleResearch ArticleAdultmedicine.medical_specialtyArticle SubjectNitrosationNitric OxidePathophysiology03 medical and health sciencesErk1/2Internal medicinePlacentamedicineHumanslcsh:QH573-671Protein kinase BPregnancyFetusNitratesS-NitrosothiolsCesarean SectionCell BiologyPeroxiredoxinsmedicine.diseaseProtein s-nitrosylationDiabetes Gestational030104 developmental biologyEndocrinologyOxidative stressCase-Control Studiesbiology.proteinPeroxiredoxinProto-Oncogene Proteins c-aktOxidative Medicine and Cellular Longevity
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Maternal and fetal genetic contribution to gestational weight gain

2018

Background: Clinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG. Participants and methods: A genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspri…

0301 basic medicineAmniotic fluidEpidemiologyEndocrinology Diabetes and MetabolismEmbaràsMedicine (miscellaneous)Genome-wide association studyBLOOD-PRESSUREType 2 diabetes030204 cardiovascular system & hematology/dk/atira/pure/core/keywords/icepCOMMON SNPSGenètica mèdica0302 clinical medicinePregnancyWeight managementOFFSPRING ADIPOSITYMass index11 Medical and Health Sciences2. Zero hunger0303 health sciencesNutrition and DieteticsObstetricsHERITABILITYMedical geneticsta3141ASSOCIATIONGestational Weight Gainddc:3. Good healthGestational diabetesCHILDREN ALSPACmedicine.anatomical_structurePREGNANCYOBESITYMENDELIAN RANDOMIZATIONGestationOriginal ArticleFemaleICEPmedicine.symptomLife Sciences & Biomedicine13 EducationTRAITSmedicine.medical_specialtyOffspringBirth weightPes corporalDevelopmentBiology03 medical and health sciencesEndocrinology & MetabolismFetusPlacentaInternal medicinemedicineJournal ArticleHumans030304 developmental biologyFetusPregnancyScience & TechnologyNutrition & Dieteticsbusiness.industryta3121Body weightmedicine.diseaseta3123BIRTH-WEIGHTBODY-MASS INDEX030104 developmental biologyEndocrinologybusinessBody mass indexWeight gainHUMAN HEIGHTGenome-Wide Association Study
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In vitro effects of vitamins C and E, n-3 and n-6 PUFA and n-9 MUFA on placental cell function and redox status in type 1 diabetic pregnant women.

2016

IF 2.972; International audience; The aim of this investigation was to determine the in vitro effects of vitamin C and E, n-3 and n-6 PUFA and n-9 MUFA on placental cell proliferation and function in type 1 diabetes. Placenta tissues were collected from 30 control healthy and 30 type 1 diabetic women at delivery. Placental cells were isolated and were cultured in RPMI medium supplemented with vitamin C (50 μM), vitamin E (50 μM), n-3 PUFA (100 μM), n-6 PUFA (100 μM) or n-9 MUFA (100 μM). Cell proliferation, cell glucose uptake and intracellular oxidative status were investigated. Our results showed that basal placental cell proliferation, glucose uptake, malondialdehyde (MDA) and carbonyl p…

0301 basic medicineAntioxidantGlucose uptakemedicine.medical_treatmentPlacentaProliferationPregnancy in DiabeticsAscorbic Acidmedicine.disease_causeAntioxidantsFatty Acids Monounsaturatedchemistry.chemical_compound0302 clinical medicinePregnancyMalondialdehydeVitamin EVitamin C[ SDV.MHEP.GEO ] Life Sciences [q-bio]/Human health and pathology/Gynecology and obstetrics030219 obstetrics & reproductive medicineTrophoblastObstetrics and Gynecologyfood and beveragesCatalasemedicine.anatomical_structureType 1 diabetes[ SDV.BDLR ] Life Sciences [q-bio]/Reproductive BiologyHypertensionFemalelipids (amino acids peptides and proteins)Oxidant/antioxidant statusOxidation-ReductionIntracellularPolyunsaturated fatty-acidsVitaminAdultRiskmedicine.medical_specialtyPlacental cellsBiology03 medical and health sciencesYoung AdultInternal medicinePlacentaFatty Acids Omega-6Fatty Acids Omega-3medicineHumans[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyCell ProliferationVitamin CSuperoxide DismutaseVitamin EMellitusPreeclampsiaDiet030104 developmental biologyEndocrinologyDiabetes Mellitus Type 1MetabolismReproductive MedicinechemistryOxidative stressOxidative stressPUFADevelopmental Biology
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The embryo-placental CD15-positive "vasculogenic zones" as a source of propranolol-sensitive pediatric vascular tumors.

2015

Abstract Objective Propranolol-induced involution is a unique biological feature of some pediatric vascular tumors, for instance infantile hemangioma (IH), cerebral cavernoma or chorioangioma. Currently, the cellular origin of these distinct tumors is unclear. In this study, we tested the hypothesis that propranolol-responsive vascular tumors are derived from common vessel-forming CD15 + progenitor cells which occur in early gestation. The aim of this study was to identify the tumor-relevant CD15 + progenitors at the early stages of embryo-placental development. Materials and methods Human embryo-placental units of 4–8 weeks gestation and pediatric vascular tumors were tested for expression…

0301 basic medicineCD31Pathologymedicine.medical_specialtyPlacentaCD34Lewis X AntigenCD15BiologyHemangioma03 medical and health sciences0302 clinical medicineNeoplastic Syndromes HereditaryPregnancyPlacentamedicineHumansCell LineageHemangioma CapillaryAge of OnsetStem Cell NicheChildNeural tubeInfant NewbornObstetrics and GynecologyPlacentationEndothelial Cellsmedicine.diseaseEmbryo MammalianPropranololPlacentationPregnancy Trimester First030104 developmental biologymedicine.anatomical_structureReproductive MedicineDrug Resistance Neoplasm030220 oncology & carcinogenesisNeoplasms Vascular TissueNeoplastic Stem CellsFemaleHemangiomaImmunostainingDevelopmental BiologyPlacenta
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Immaturity for gestational age of microvasculature and placental barrier in term placentas with high weight

2017

Abstract Objective Villous immaturity for gestational age is a multifactorial developmental deviation associated with unexpected placental insufficiency, fetal hypoxia and term fetal death. In our previous work we have shown that immature CD15+/CD31+/CD34+ endothelial cells were an important indicator of placental villous immaturity and chronic insufficiency. The aim of this study was to perform a comparative analysis of CD15-marked immaturity in the vessel walls between normal and pathological term placentas of clinically and structurally heterogenous groups with normal, low and high weight. Study design 165 clinically normal and pathological placentas of gestational age 39–42 with normal …

0301 basic medicineCD31medicine.medical_specialtyTerm BirthPlacentaCD34Lewis X AntigenGestational AgePlacental insufficiency03 medical and health sciences0302 clinical medicineVasculogenesisImmunophenotypingPregnancyInternal medicinemedicineHumansPlacental villous immaturityFetus030219 obstetrics & reproductive medicinebusiness.industryObstetrics and GynecologyGestational ageOrgan SizePlacental Insufficiencymedicine.disease030104 developmental biologyEndocrinologyReproductive MedicineMicrovesselsImmunologyFemaleEndothelium VascularbusinessEuropean Journal of Obstetrics & Gynecology and Reproductive Biology
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Transcriptome of early embryonic invasion at implantation sites in a murine model

2015

Successful implantation relies on the interaction between a competent embryo and a receptive endometrium. The aim of the present study was to investigate genes differentially expressed in early invasive embryonic tissue versus decidual tissue in mice. Samples were obtained from the ectoplacental cone, the immediately surrounding deciduas and from deciduas from interimplantation sites. Microarray analysis showed that 817 genes were differentially expressed between extra-embryonic tissue and the surrounding decidua and that 360 genes were differentially expressed between the different deciduas, with a high representation of developmental processes. Genes differentially expressed in the matern…

0301 basic medicineDECIDUAL TISSUEECTOPLACENTAL CONEOtras Ciencias BiológicasReproductive technologyBiologyMOUSE IMPLANTATIONTROPHOBLAST INVASIONCiencias BiológicasTranscriptome03 medical and health sciences0302 clinical medicineEndocrinologyMICROARRAYGeneticsmedicineCompartment (development)Molecular Biology030219 obstetrics & reproductive medicineMicroarray analysis techniquesDeciduaEmbryogenesisEmbryonic TissueEmbryonic stem cellCell biology030104 developmental biologymedicine.anatomical_structureRNA EXPRESSION PATTERNSReproductive Medicineembryonic structuresImmunologyAnimal Science and ZoologyCIENCIAS NATURALES Y EXACTASDevelopmental BiologyBiotechnologyReproduction, Fertility and Development
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Methylmercury-induced developmental toxicity is associated with oxidative stress and cofilin phosphorylation. Cellular and human studies

2017

Environmental exposure to methylmercury (MeHg) during development is of concern because it is easily incorporated in children’s body both pre- and post-natal, it acts at several levels of neural pathways (mitochondria, cytoskeleton, neurotransmission) and it causes behavioral impairment in child. We evaluated the effects of prolonged exposure to 10–600 nM MeHg on primary cultures of mouse cortical (CCN) and of cerebellar granule cells (CGC) during their differentiation period. In addition, it was studied if prenatal MeHg exposure correlated with altered antioxidant defenses and cofilin phosphorylation in human placentas (n = 12) from the INMA cohort (Spain). Exposure to MeHg for 9 days in v…

0301 basic medicineDevelopmental DisabilitiesGlutathione reductaseCiencias de la SaludMitochondrionMETHYLMERCURYToxicologymedicine.disease_causeProtein CarbonylationMiceCytosolMITOCHONDRIAPregnancyPhosphorylationOXIDATIVE STRESSCells Culturedchemistry.chemical_classificationNeuronsbiologyGeneral NeuroscienceGlutathione peroxidaseCOFILINBrainMethylmercuryEnvironmental exposureCofilinMethylmercury CompoundsMitochondrial Proton-Translocating ATPasesGlutathioneCell biologyMitochondriaGlutathione ReductaseActin Depolymerizing FactorsCofilinPhosphorylationFemaleHuman placentaactinCortactinCIENCIAS MÉDICAS Y DE LA SALUDmacromolecular substancesACTIN03 medical and health sciencesCultured neuronsmedicineAnimalsHumansCULTURED NEURONSGlutathione PeroxidaseSalud OcupacionalHUMAN PLACENTAMolecular biology030104 developmental biologychemistryAnimals NewbornOxidative stressbiology.proteinOxidative stress
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Prenatal exposure to mixtures of xenoestrogens and genome-wide DNA methylation in human placenta

2015

BACKGROUND: In utero exposure to xenostrogens may modify the epigenome. We explored the association of prenatal exposure to mixtures of xenoestrogens and genome-wide placental DNA methylation. MATERIALS & METHODS: Sex-specific associations between methylation changes in placental DNA by doubling the concentration of TEXB-alpha exposure were evaluated by robust multiple linear regression. Two CpG sites were selected for validation and replication in additional male born placentas. RESULTS: No significant associations were found, although the top significant CpGs in boys were located in the LRPAP1, HAGH, PPARGC1B, KCNQ1 and KCNQ1DN genes, previously associated to birth weight, Type 2 diabetes…

0301 basic medicineMaleCancer Researchmedicine.medical_specialtymedicine.medical_treatmentPlacentaADNBiologyEpigenesis GeneticAndrology03 medical and health scienceschemistry.chemical_compoundSex FactorsPregnancyPlacentaInternal medicineGeneticsmedicineBirth WeightHumansPrenatalLDL-Receptor Related Protein-Associated ProteinGeneTEXBEndocrine disruptorsDNA methylationEpigenome xenoestrogensRNA-Binding ProteinsEstrogensMethylationEpigenomeSteroid hormone030104 developmental biologyEndocrinologymedicine.anatomical_structureXenoestrogenCpG sitechemistryPrenatal Exposure Delayed EffectsDNA methylationKCNQ1 Potassium ChannelProgrammingCpG IslandsFemaleThiolester HydrolasesCarrier ProteinsGenome-Wide Association Study
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