0000000000191121

AUTHOR

Andrés Laguna-fernandez

0000-0002-0066-7222

showing 7 related works from this author

Estradiol induces endothelial cell migration and proliferation through estrogen receptor-enhanced RhoA/ROCK pathway

2010

Migration and proliferation of endothelial cells are involved in re-endothelialization and angiogenesis, two important cardiovascular processes that are increased in response to estrogens. RhoA, a small GTPase which controls multiple cellular processes, is involved in the control of cell migration and proliferation. Our aim was to study the role of RhoA on estradiol-induced migration and proliferation and its dependence on estrogen receptors activity. Human umbilical vein endothelial cells were stimulated with estradiol, in the presence or absence of ICI 182780 (estrogen receptors antagonist) and Y-27632 (Rho kinase inhibitor). Estradiol increased Rho GEF-1 gene expression and RhoA (gene an…

MaleTranscriptional ActivationRHOAAngiogenesismedicine.drug_classEstrogen receptorCell Cycle ProteinsBiochemistryUmbilical CordEndocrinologyCell MovementmedicineHumansReceptorMolecular BiologyCells CulturedCell ProliferationEnzyme Assaysrho-Associated KinasesEstradiolbiologyChemistryEndothelial CellsCell migrationUp-RegulationCell biologyEndothelial stem cellReceptors EstrogenRho kinase inhibitorEstrogenCancer researchbiology.proteinFemalerhoA GTP-Binding Proteinhormones hormone substitutes and hormone antagonistsSignal TransductionMolecular and Cellular Endocrinology
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Estradiol Stimulates Vasodilatory and Metabolic Pathways in Cultured Human Endothelial Cells

2009

Vascular effects of estradiol are being investigated because there are controversies among clinical and experimental studies. DNA microarrays were used to investigate global gene expression patterns in cultured human umbilical vein endothelial cells (HUVEC) exposed to 1 nmol/L estradiol for 24 hours. When compared to control, 187 genes were identified as differentially expressed with 1.9-fold change threshold. Supervised principal component analysis and hierarchical cluster analysis revealed the differences between control and estradiol-treated samples. Physiological concentrations of estradiol are sufficient to elicit significant changes in HUVEC gene expression. Notch signaling, actin cyt…

medicine.medical_specialtyUmbilical Veinsmedicine.drug_classScienceEstrogen receptorBiologyAmidohydrolasesTransforming Growth Factor beta1chemistry.chemical_compoundInternal medicinemedicineCluster AnalysisEstrogen Receptor betaHumansEstrogen receptor betaCell Biology/Gene ExpressionCells CulturedOligonucleotide Array Sequence AnalysisRegulation of gene expressionPrincipal Component AnalysisMultidisciplinaryEstradiolPhysiology/EndocrinologyReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingQPhysiology/Cardiovascular Physiology and CirculationREstrogen Receptor alphaEndothelial CellsReproducibility of ResultsActin cytoskeletonVasodilationEndocrinologychemistryGene Expression RegulationEstrogenCyclooxygenase 1MedicineSignal transductionAsymmetric dimethylarginineEstrogen receptor alphahormones hormone substitutes and hormone antagonistsMetabolic Networks and PathwaysResearch ArticleSignal TransductionPLoS ONE
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Estradiol, acting through estrogen receptor alpha, restores dimethylarginine dimethylaminohydrolase activity and nitric oxide production in oxLDL-tre…

2011

Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthase. ADMA accumulation, mainly due to a decreased dimethylarginine dimethylaminohydrolase (DDAH) activity, has been related to the development of cardiovascular diseases. We investigate whether estradiol prevents the changes induced by oxidized low density lipoprotein (oxLDL) on the DDAH/ADMA/NO pathway in human umbilical artery endothelial cells (HUAEC). HUAEC were exposed to estradiol, native LDL (nLDL), oxLDL and their combinations for 24 h. In some experiments, cells were also exposed to the unspecific estrogen receptor (ER) antagonist ICI 182780, the specific ERα antagonist MPP or specific agonists …

medicine.medical_specialtyProtein-Arginine N-MethyltransferasesEndotheliumNitric Oxide Synthase Type IIImedicine.drug_classBlotting WesternArginineNitric OxideBiochemistryUmbilical ArteriesNitric oxideAmidohydrolasesReceptors G-Protein-Coupledchemistry.chemical_compoundEndocrinologyEnosInternal medicinemedicineEstrogen Receptor betaHumansEstrogens Non-SteroidalMolecular BiologyCells CulturedbiologyEstradiolArtèriesProtein StabilityEstrogen AntagonistsEstrogen Receptor alphaEndoteli vascularbiology.organism_classificationNitric oxide synthaseIsoenzymesLipoproteins LDLRepressor Proteinsmedicine.anatomical_structureEndocrinologychemistryReceptors EstrogenEstrogenbiology.proteinlipids (amino acids peptides and proteins)Endothelium VascularAsymmetric dimethylarginineEstrogen receptor alphaGPER
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Endothelial transcriptomic changes induced by oxidized low density lipoprotein disclose an up-regulation of Jak-Stat pathway.

2015

Oxidized low density lipoproteins (oxLDLs) act as an etiological factor in the development of atherosclerosis by modifying the biological properties of endothelial cells through mechanisms of vascular inflammation. To deepen the oxLDL changes at cellular level, a transcriptomic analysis of human umbilical artery endothelial cells (HUAECs) treated with oxLDL was performed to identify the modified signaling pathways. Total RNA was isolated from HUAECs treated with oxLDL (100 μg/ml). Gene expression analysis was carried out using Affymetrix oligonucleotide microarrays. Biological pathway analysis was performed using Ingenuity Pathway Analysis software. Microarray assay demonstrated that oxLDL …

Cell signalingTime FactorsPhysiologyBlotting WesternBiologyReal-Time Polymerase Chain ReactionTransfectionGene Expression Regulation EnzymologicBiological pathwayTranscriptomeRNA interferenceGene expressionHuman Umbilical Vein Endothelial CellsHumansGene Regulatory NetworksProtein Kinase InhibitorsCells CulturedOligonucleotide Array Sequence AnalysisPharmacologyGene Expression ProfilingJAK-STAT signaling pathwaySTAT2 Transcription FactorJanus Kinase 1Janus Kinase 2Cell biologyEndothelial stem cellLipoproteins LDLSTAT1 Transcription FactorMolecular Medicinelipids (amino acids peptides and proteins)RNA InterferenceSignal transductionTranscriptomeSignal TransductionVascular pharmacology
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Gene expression profile induced by ovariectomy in bone marrow of mice: a functional approach to identify new candidate genes associated to osteoporos…

2013

Osteoporosis is a multifactorial skeletal pathology with a main genetic component. To date, however, the majority of genes associated with this pathology remain unknown since genes cataloged to date only explain a part of the heritability of bone phenotypes. In the present study, we have used a genome-wide gene expression approach by means of microarrays to identify new candidate genes involved in the physiopathology of osteoporosis, using as a model the ovariectomized (OVX) mice by comparing global bone marrow gene expression of the OVX mice with those of SHAM operated mice. One hundred and eighty transcripts were found to be differentially expressed between groups. The analysis showed 23 …

Candidate genemedicine.medical_specialtyHistologyGPX3PhysiologyEndocrinology Diabetes and MetabolismOsteoporosisSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideBone remodelingMiceBone DensityBone MarrowInternal medicineGene expressionmedicineAnimalsHumansGeneOligonucleotide Array Sequence AnalysisGene Expression Profilingmedicine.diseaseMice Inbred C57BLEndocrinologyOvariectomized ratOsteoporosisFemaleBone
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Progestogens reduce thromboxane production by cultured human endothelial cells.

2011

Objectives Progestogens have been poorly studied concerning their roles in endothelial physiology. Prostanoids are vasoactive compounds, such as thromboxane A2, a potent vasoconstrictor, and prostacyclin, a vasodilator. We examined the effects of two progestogens used clinically, progesterone and medroxyprogesterone acetate, on thromboxane A2 production by cultured human umbilical vein endothelial cells (HUVEC) and investigated the role of progesterone receptors and the enzymes involved in production of thromboxane A2 and prostacyclin. Methods Cells were exposed to 1‐100 nmol/l of either progesterone or medroxyprogesterone acetate, and thromboxane A2 production was measured in culture mediu…

medicine.medical_specialtyUmbilical VeinsAntineoplastic Agents HormonalThromboxaneBlotting WesternGene ExpressionProstacyclinMedroxyprogesterone AcetatePolymerase Chain ReactionProstacyclin synthaseThromboxane receptorThromboxane ProductionThromboxane A2chemistry.chemical_compoundThromboxane A2Hormone AntagonistsCytochrome P-450 Enzyme SystemInternal medicineProgesterone receptorMedicineHumansCyclooxygenase InhibitorsRNA MessengerCells CulturedProgesteronebiologyDose-Response Relationship Drugbusiness.industryObstetrics and GynecologyEndothelial CellsGeneral MedicineIntramolecular OxidoreductasesThromboxane B2MifepristoneEndocrinologychemistrycardiovascular systembiology.proteinPyrazolesThromboxane-A synthaseThromboxane-A SynthaseProgestinsbusinessmedicine.drugClimacteric : the journal of the International Menopause Society
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Estradiol selectively stimulates endothelial prostacyclin production through estrogen receptor-α

2010

Estradiol (E2) acts on the endothelium to promote vasodilatation through the release of several compounds, including prostanoids, which are products of arachidonic acid metabolism. Among these, prostacyclin (PGI2) and thromboxane A2 (TXA2) exert opposite effects on vascular tone. The role of different estrogen receptors (ERs) in the PGI2/TXA2 balance, however, has not been fully elucidated. Our study sought to uncover whether E2 enhances basal production of PGI2 or TXA2 in cultured human umbilical vein endothelial cells (HUVECs), to analyze the enzymatic mechanisms involved, and to evaluate the different roles of both types of ERs (ERα and ERβ). HUVECs were exposed to E2, selective ERα (1,3…

Malemedicine.medical_specialtyEndotheliumDiarylpropionitrileEstrogen receptorProstacyclinBiologyThromboxane A2chemistry.chemical_compoundThromboxane A2EndocrinologyCytochrome P-450 Enzyme SystemInternal medicinemedicineEstrogen Receptor betaHumansMolecular BiologyCells CulturedEstradiolGroup IV Phospholipases A2Estrogen Receptor alphaEndothelial CellsProstanoidEpoprostenolIntramolecular OxidoreductasesEndocrinologymedicine.anatomical_structurechemistryCyclooxygenase 1cardiovascular systembiology.proteinFemalelipids (amino acids peptides and proteins)Endothelium VascularThromboxane-A synthaseEstrogen receptor alphamedicine.drugJournal of Molecular Endocrinology
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