Search results for "Estrogen"

showing 10 items of 530 documents

Estrogen Signaling in Bystander Foxp3 neg CD4 + T Cells Suppresses Cognate Th17 Differentiation in Trans and Protects from Central Nervous System Aut…

2018

Abstract 17β-Estradiol (E2) suppresses the development of experimental autoimmune encephalomyelitis (EAE) through estrogen receptor (ER) α, yet the cellular targets remain elusive. We have used an adoptive transfer model of myelin oligodendrocyte glycoprotein–specific CD4+ T cells from 2D2 TCR transgenic mice. We show that in the recipient mice, ERα expression in bystander CD4+ T cells, rather than in cognate 2D2 T cells, is required for the inhibition of Th17 cell differentiation by E2. Coadministration of estrogen-primed WT, but not ERα-deficient CD4+ T cells, with naive 2D2 T cells lacking ERα inhibited the development of Th17 cell–mediated EAE. Suppression of Th17 cells and protection f…

0301 basic medicineAdoptive cell transferCell growthChemistryCellular differentiation[SDV]Life Sciences [q-bio]ImmunologyExperimental autoimmune encephalomyelitisEstrogen receptorFOXP3medicine.diseaseOligodendrocyte3. Good healthCell biology03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureBystander effectmedicineImmunology and AllergyComputingMilieux_MISCELLANEOUS030215 immunology
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Genome-wide DNA methylation differences according to oestrogen receptor beta status in colorectal cancer.

2019

Involvement of sex hormones in colorectal cancer (CRC) development has been linked to oestrogen receptor β (ERβ). Expression of ERβ is found reduced in tumour tissue and inversely related to mortality. However, mechanisms are not well understood. Our study aimed to detect differentially methylated genes associated with ERβ expression, which could point to mechanisms by which ERβ could influence risk and prognosis of CRC. Epigenome-wide DNA methylation profiling was performed using Illumina HumanMethylation450k BeadChip arrays in two independent tumour sample sets of CRC patients recruited in 2003–2010 by the German DACHS study (discovery cohort n = 917, replication cohort n = 907). ERβ expr…

0301 basic medicineAdultMaleCancer ResearchColorectal cancerBiologyGenomeEpigenesis Genetic03 medical and health sciencesTumour tissue0302 clinical medicinemedicineBiomarkers TumorEstrogen Receptor betaHumansEpigeneticsOestrogen receptorBeta (finance)Promoter Regions GeneticMolecular BiologyAgedAged 80 and overDNA MethylationMiddle Agedmedicine.diseasePrognosisGene Expression Regulation NeoplasticSurvival Rate030104 developmental biology030220 oncology & carcinogenesisCase-Control StudiesDNA methylationCancer researchFemaleColorectal NeoplasmsHormoneFollow-Up StudiesGenome-Wide Association StudyResearch PaperEpigenetics
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Treatment for hereditary angioedema with normal C1-INH and specific mutations in the F12 gene (HAE-FXII).

2016

Hereditary angioedema with normal C1 esterase inhibitor and mutations in the F12 gene (HAE-FXII) is associated with skin swellings, abdominal pain attacks, and the risk of asphyxiation due to upper airway obstruction. It occurs nearly exclusively in women. We report our experience treating HAE-FXII with discontinuation of potential trigger factors and drug therapies. The study included 72 patients with HAE-FXII. Potential triggers included estrogen-containing oral contraceptives (eOC), hormonal replacement therapy, or angiotensin-converting enzyme inhibitors. Drug treatment comprised plasma-derived C1 inhibitor (pdC1-INH) for acute swelling attacks and progestins, tranexamic acid, and danaz…

0301 basic medicineAdultMalemedicine.medical_specialtyExacerbationAdolescentImmunologyAngiotensin-Converting Enzyme InhibitorsGastroenterologyChemopreventionC1-inhibitorHereditary Angioedema Type III03 medical and health sciencesYoung Adult0302 clinical medicineRisk FactorsInternal medicinemedicineImmunology and AllergyHumansHereditary Angioedema Type IIIChildAgedDanazolbiologybusiness.industryEstrogensMiddle Agedmedicine.diseaseSurgeryDiscontinuation030104 developmental biologyTreatment Outcome030228 respiratory systemQuinaprilHereditary angioedemaFactor XIIMutationbiology.proteinDisease ProgressionFemalebusinessComplement C1 Inhibitor ProteinTranexamic acidBiomarkersmedicine.drugAllergy
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Analysis of cold activation of the contact system in hereditary angioedema with normal C1 inhibitor.

2021

Hereditary angioedema (HAE) attacks are caused by excessive activation of the contact system. Understanding how the contact system is activated in HAE, especially in patients with normal C1 inhibitor (HAEnCI), is essential to effectively treat this disease. Contact system activation involves the cleavage of several proteins including Factor XII (FXII), high molecular weight kininogen (HK), prekallikrein, sgp120 (ITIH4) and C1 inhibitor (C1-INH) before the subsequent generation of bradykinin that mediates HAE. In this study, we evaluated the fragmentation and enzymatic activity of contact system proteins in HAEnCI plasma samples before and after contact system activation induced by incubatio…

0301 basic medicineAdultMalemedicine.medical_specialtyHigh-molecular-weight kininogenImmunologyProteinase Inhibitory Proteins SecretoryBradykininBradykininC1-inhibitorHereditary Angioedema Type III03 medical and health scienceschemistry.chemical_compoundYoung Adult0302 clinical medicineInternal medicinemedicineHumansFragmentation (cell biology)Molecular BiologyBlood CoagulationFactor XIIbiologyKininogensPrekallikreinPrekallikreinEstrogensPlasminogenKallikreinMiddle Agedmedicine.diseaseCold Temperature030104 developmental biologyEndocrinologychemistryHereditary angioedemaFactor XIIbiology.proteinFemaleKallikreinsComplement C1 Inhibitor Protein030215 immunologyMolecular immunology
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Role of miRNA in the Regulatory Mechanisms of Estrogens in Cardiovascular Ageing

2018

Cardiovascular diseases are a worldwide health problem and are the leading cause of mortality in developed countries. Together with experimental data, the lower incidence of cardiovascular diseases in women than in men of reproductive age points to the influence of sex hormones at the cardiovascular level and suggests that estrogens play a protective role against cardiovascular disease and that this role is also modified by ageing. Estrogens affect cardiovascular function via their specific estrogen receptors to trigger gene expression changes at the transcriptional level. In addition, emerging studies have proposed a role for microRNAs in the vascular effects mediated by estrogens. miRNAs …

0301 basic medicineAgingEstrogen receptorFisiologiaDiseaseReview Article030204 cardiovascular system & hematologyBioinformaticsBiochemistry03 medical and health sciences0302 clinical medicineGene expressionmicroRNAMedicineAnimalsHumanslcsh:QH573-671GeneSistema cardiovascularRegulation of gene expressionlcsh:Cytologybusiness.industryEstrogensCell BiologyGeneral MedicineMicroRNAs030104 developmental biologyGene Expression RegulationAgeingCardiovascular DiseasesbusinessHormone
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Decreased bioavailability of nitric oxide in aorta from ovariectomized senescent mice. Role of cyclooxygenase.

2015

This study investigates the effects of aging and/or ovariectomy on vascular reactivity to thromboxane A2 (TXA2) receptor stimulation with U46619, and the modulation by nitric oxide (NO) and cyclooxygenase (COX) in aorta from female senescence-accelerated mice (SAMP8) and from senescence resistant mice (SAMR1). Five-month-old female SAMR1 and SAMP8 were divided into three groups: sham-operated, ovariectomized and ovariectomized plus estradiol. Twenty-eight days after surgery, thoracic aortic rings were mounted for isometric recording of tension and concentration-response curves for U46619 (10(-10)-3 × 10(-7) M) were performed in the absence and in the presence of the NO synthase inhibitor N(…

0301 basic medicineAgingReceptors ThromboxaneAorta Thoracic030204 cardiovascular system & hematologyBiochemistrychemistry.chemical_compoundThromboxane A2Mice0302 clinical medicineEndocrinologySuperoxidesThoracic aortaVasoconstrictor AgentsbiologyEstradiolSuperoxideEstrogen Replacement TherapyAge FactorsOvariectomized ratFemaleMenopauseSignal Transductionmedicine.medical_specialtymedicine.drug_classOvariectomyDown-RegulationNitric OxideNitric oxide03 medical and health sciencesThromboxane A2medicine.arteryInternal medicineGeneticsmedicineAnimalsCyclooxygenase InhibitorsMolecular BiologyAortaDose-Response Relationship Drugbusiness.industryCell BiologyEnzyme ActivationOxidative Stress030104 developmental biologyEndocrinologychemistryEstrogenProstaglandin-Endoperoxide SynthasesVasoconstrictionbiology.proteinCyclooxygenaseNitric Oxide SynthasebusinessExperimental gerontology
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Estrogenic regulation of skeletal muscle proteome : a study of premenopausal women and postmenopausal MZ cotwins discordant for hormonal therapy

2017

Female middle age is characterized by a decline in skeletal muscle mass and performance, predisposing women to sarcopenia, functional limitations, and metabolic dysfunction as they age. Menopausal loss of ovarian function leading to low circulating level of 17b-estradiol has been suggested as a contributing factor to aging-related muscle deterioration. However, the underlying molecular mechanisms remain largely unknown and thus far androgens have been considered as a major anabolic hormone for skeletal muscle. We utilized muscle samples from 24 pre- and postmenopausal women to establish proteome-wide profiles, associated with the difference in age (30–34 years old vs. 54– 62 years old), men…

0301 basic medicineAgingnaisetlabel‐free protein quantitationProteomeAnabolismvaihdevuodetmedicine.medical_treatmentTwinsmenopausenano‐LC‐HD‐MSElihakset0302 clinical medicineSTRENGTHBRAIN315 Sport and fitness sciencesta315luustoINHIBITORHormone replacement therapy (menopause)ta3142MITOCHONDRIAL BIOGENESISMiddle AgedPostmenopauseMenopauseREPLACEMENThormone replacement therapyEditorialmedicine.anatomical_structurehormonihoitoHormonal therapyOriginal ArticleFemalemuscleswomenAdultestrogeenitnano-LC-HD-MSEEXPRESSIONmedicine.medical_specialtyBiologyestrogenic regulation03 medical and health sciencesmitochondrial functionInternal medicinemedicineHumansMuscle Skeletallabel-free protein quantitationmuscle proteomeAgedSkeletal muscleEstrogenslabel-free proteinquantitationOriginal ArticlesCell Biologyfunctional annotationmedicine.diseaseMiddle ageMONOZYGOTIC TWIN PAIRS030104 developmental biologyEndocrinologyPremenopauselihasmassaSarcopeniaCELLS3111 BiomedicineEnergy Metabolismfemale muscle030217 neurology & neurosurgeryskeletal musclesHormone
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A Computational Assay of Estrogen Receptor α Antagonists Reveals the Key Common Structural Traits of Drugs Effectively Fighting Refractory Breast Can…

2017

AbstractSomatic mutations of the Estrogen Receptor α (ERα) occur with an up to 40% incidence in ER sensitive breast cancer (BC) patients undergoing prolonged endocrine treatments. These polymorphisms are implicated in acquired resistance, disease relapse, and increased mortality rates, hence representing a current major clinical challenge. Here, multi-microseconds (12.5 µs) molecular dynamics simulations revealed that recurrent ERα polymorphisms (i. e. L536Q, Y537S, Y537N, D538G) (mERα) are constitutively active in their apo form and that they prompt the selection of an agonist (active)-like conformation even upon antagonists binding. Interestingly, our simulations rationalize, for the firs…

0301 basic medicineAgonistModels MolecularBreast cancerComputational chemistryMolecular dynamicsSomatic cellmedicine.drug_classlcsh:MedicineEstrogen receptorBreast Neoplasms-Molecular Dynamics SimulationPolymorphism Single NucleotideArticleProtein Structure SecondaryEstrogen Receptor Antagonists03 medical and health sciences0302 clinical medicineBreast cancermedicineEndocrine systemHumanslcsh:ScienceMultidisciplinarybusiness.industrylcsh:REstrogen Receptor alphamedicine.diseaseEstrogen Receptor Antagonist030104 developmental biologySelective estrogen receptor modulator030220 oncology & carcinogenesisCancer researchlcsh:QFemaleEstrogen Receptor AntagonistsbusinessEstrogen receptor alphaBreast NeoplasmHuman
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Estradiol, acting through ERα, induces endothelial non-classic renin-angiotensin system increasing angiotensin 1–7 production

2016

Intracellular renin-angiotensin system (RAS) can operate independently of the circulating RAS. Estrogens provide protective effects by modulating the RAS. Our aim was to investigate the effect of estradiol (E2) on angiotensin converting enzymes (ACE) 1 and ACE2 expression and activities in human endothelial cells (HUVEC), and the role of estrogen receptors (ER). The results confirmed the presence of active intracellular RAS in HUVEC. Physiological concentrations of E2 induced a concentration-dependent increase of ACE1 and ACE2 mRNA expression and ACE1, but not ACE2, protein levels. ACE1 and ACE2 enzymatic activities were also induced with E2. These effects were mediated through ERα activati…

0301 basic medicineAgonistmedicine.medical_specialtymedicine.drug_classEstrogen receptorPeptidyl-Dipeptidase A030204 cardiovascular system & hematologyBiologyBiochemistryEstrogen Receptor AntagonistsCiencias Biológicas03 medical and health sciences0302 clinical medicineEndocrinologyPiperidinesInternal medicineRenin–angiotensin systemHuman Umbilical Vein Endothelial CellsmedicineHumansFulvestrantMolecular BiologyESTROGEN RECEPTORDose-Response Relationship DrugEstradiolEstrogen Receptor alphaANGIOTENSIN CONVERTING ENZYMESBioquímica y Biología MolecularRENIN ANGIOTENSIN SYSTEMPeptide FragmentsEndothelial stem cellESTROGEN030104 developmental biologyEndocrinologyGene Expression RegulationEstrogenENDOTHELIAL CELLPyrazolesAngiotensin-Converting Enzyme 2Estrogen Receptor AntagonistsAngiotensin IEstrogen receptor alphaCIENCIAS NATURALES Y EXACTAShormones hormone substitutes and hormone antagonistsIntracellularMolecular and Cellular Endocrinology
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Cytotoxic effects of zearalenone and its metabolites and antioxidant cell defense in CHO-K1 cells.

2016

Zearalenone (ZEA) and its metabolites (α-zearalenol; α-ZOL, β-zearalenol; β-ZOL) are secondary metabolites of Fusarium fungi that produce cell injury. The present study explores mycotoxin-induced cell damage and cellular protection mechanisms in CHO-K1 cells. Cytotoxicity has been determined by reactive oxygen species (ROS) production and DNA damage. ROS production was determined using the fluorescein assay and DNA strand breakage by comet assay. Intracellular protection systems were glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD). The results demonstrated that all mycotoxins increased the ROS levels up to 5.3-fold the control levels in CHO-K1 …

0301 basic medicineAntioxidantDNA damagemedicine.medical_treatmentImmunoblottingCHO CellsToxicologyAntioxidantsSuperoxide dismutase03 medical and health scienceschemistry.chemical_compoundCricetulusCricetinaemedicineAnimalsEstrogens Non-SteroidalCell damagechemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidasebiologySuperoxide DismutaseGlutathione peroxidasefood and beveragesGeneral MedicineGlutathionemedicine.diseaseCatalaseGlutathioneComet assay030104 developmental biologychemistryBiochemistrybiology.proteinZearalenoneZeranolComet AssayReactive Oxygen SpeciesOxidation-ReductionFood ScienceDNA DamageFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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