Search results for "Inducible"

showing 10 items of 111 documents

Retinoic acid inhibits nitric oxide synthase-2 expression through the retinoic acid receptor-alpha.

2000

Retinoids are multipotent modulators of cellular functions and suppress cytokine-induced production of nitric oxide (NO) in several cell types. We have explored the mechanisms by which retinoic acid (RA) regulates NO production in rat aortic smooth muscle cells (VSMC), which express NOS2 in response to proinflammatory cytokines. RA inhibited interleukin-1beta (IL-1beta)-induced NOS2 mRNA expression and NO production. These effects were attenuated by the retinoic acid receptor (RAR) antagonist CD3106, indicating that they were mediated through retinoic acid receptors (RARs). The synthetic retinoid agonists CD336 (which specifically binds RARalpha) and CD367 (which binds all RARs) but not ago…

MaleTranscription GeneticReceptors Retinoic AcidBiophysicsRetinoic acidNitric Oxide Synthase Type IIRetinoic acid receptor betaAorta ThoracicTretinoinBiochemistryGene Expression Regulation EnzymologicMuscle Smooth VascularProinflammatory cytokineRetinoic acid-inducible orphan G protein-coupled receptorRats Sprague-Dawleychemistry.chemical_compoundparasitic diseasesAnimalsPromoter Regions GeneticMolecular BiologyCells CulturedbiologyRetinoic Acid Receptor alphaNitric oxide synthase 2Cell BiologyRetinoic acid receptor gammarespiratory systemCell biologyRatsRetinoic acid receptorKineticsBiochemistrychemistryRetinoic acid receptor alphabiology.proteinNitric Oxide SynthaseInterleukin-1Biochemical and biophysical research communications
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2-Methoxyestradiol confers neuroprotection and inhibits a maladaptive HIF-1α response after traumatic brain injury in mice

2014

HIF-1α is pivotal for cellular homeostasis in response to cerebral ischemia. Pharmacological inhibition of HIF-1α may reduce secondary brain damage by targeting post-translational mechanisms associated with its proteasomal degradation and nuclear translocation. This study examined the neuroprotective effects of 2-methoxyestradiol (2ME2), the involved HIF-1α-dependent response, and alternative splicing in exon 14 of HIF-1α (HIF-1α∆Ex14) after traumatic brain injury (TBI) in mice. Intraperitoneal 2ME2 administration 30 min after TBI caused a dose-dependent reduction in secondary brain damage after 24 h. 2ME2 was physiologically tolerated, showed no effects on immune cell brain migration, and …

MaleTraumatic brain injuryBlotting WesternIschemiaCellular homeostasisBrain damagePharmacologyBiologyBiochemistryNeuroprotectionBrain IschemiaMitochondrial ProteinsMiceCellular and Molecular Neurosciencechemistry.chemical_compoundPlasminogen Activator Inhibitor 1medicineAnimalsCell NucleusNeuronsEstradiolTumor Necrosis Factor-alphaAlternative splicingMembrane ProteinsExonsHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseImmunohistochemistryUp-RegulationMice Inbred C57BLAlternative SplicingProtein TransportNeuroprotective AgentsGene Expression RegulationchemistryBrain InjuriesPlasminogen activator inhibitor-1Tumor necrosis factor alphamedicine.symptomNeuroscienceInjections IntraperitonealSubcellular FractionsJournal of Neurochemistry
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HIF-1α and HIF-2α Are Differentially Regulated In vivo in Neuroblastoma: High HIF-1α Correlates Negatively to Advanced Clinical Stage and Tumor Vascu…

2009

Abstract Purpose: Hypoxia is considered to be a major driving force behind tumor angiogenesis. The stabilization and activation at hypoxia of the hypoxia-inducible factors HIF-1α and HIF-2α and the concomitant induction of expression of vascular endothelial growth factor (VEGF) and other proangiogenic factors provide a molecular frame for hypoxia-driven tumor angiogenesis. This study has investigated how HIF and VEGF protein levels relate to each other with regard to vascularization, tumor stage, and overall survival in neuroblastoma. Experimental Design: Tissue cores taken from tumor specimens representing 93 children with neuroblastoma were arranged on a microarray and stained for HIF-1α,…

MaleVascular Endothelial Growth Factor ACD31Cancer ResearchPathologymedicine.medical_specialtyBiologyModels BiologicalNeovascularizationchemistry.chemical_compoundIn vivoNeoplasmsNeuroblastomaBasic Helix-Loop-Helix Transcription FactorsmedicineHumansHypoxiaRegulation of gene expressionNeovascularization PathologicInfantCancerHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseGene Expression Regulation NeoplasticPlatelet Endothelial Cell Adhesion Molecule-1Vascular endothelial growth factorTreatment OutcomeHIF1AOncologychemistryChild PreschoolCancer researchFemalemedicine.symptomClinical Cancer Research
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Lactate: mirror and motor of tumor malignancy

2004

A number of studies have shown that malignant transformation is associated with an increase in glycolytic flux and in anaerobic and aerobic cellular lactate excretion. Using quantitative bioluminescence imaging in various primary carcinomas in patients (uterine cervix, head and neck, colorectal region) at first diagnosis of the disease, we showed that lactate concentrations in tumors in vivo can be relatively low or extremely high (up to 40 micromol/g) in different individual tumors or within the same lesion. In all tumor entities investigated, high concentrations of lactate were correlated with a high incidence of distant metastasis already in an early stage of the disease. Low lactate tum…

MaleVascular Endothelial Growth Factor ACancer ResearchPathologymedicine.medical_specialtyMalignancyMalignant transformationchemistry.chemical_compoundNeoplasmsLactate dehydrogenasemedicineHumansBioluminescence imagingRadiology Nuclear Medicine and imagingGlycolysisLactic AcidHyaluronic AcidNeoplasm MetastasisL-Lactate Dehydrogenasebusiness.industryHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseCell HypoxiaUp-RegulationVascular endothelial growth factorCell Transformation NeoplasticOncologychemistryCancer cellFemalebusinessAnaerobic exerciseTranscription FactorsSeminars in Radiation Oncology
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Atrial fibrillation is associated with cardiac hypoxia.

2008

BACKGROUND: Atrial fibrillation (AF), the most common human arrhythmia, is responsible for substantial morbidity and mortality and may be promoted by selective atrial ischemia and atrial fibrosis. Consequently, we investigated markers for hypoxia and angiogenesis in AF. METHODS: Right atrial appendages (n=158) were grouped according to heart rhythm [sinus rhythm (SR) or AF]. The degree of fibrosis and microvessel density of all patients were determined morphometrically using Sirius-Red- and CD34/CD105-stained sections, respectively. Next, sections (n=77) underwent immunostaining to detect hypoxia- and angiogenesis-related proteins [hypoxia-inducible factor (HIF)1 alpha, HIF2 alpha, vascular…

MaleVascular Endothelial Growth Factor Amedicine.medical_specialtyCytoplasmAngiogenesisIschemiaMyocardial IschemiaBiologyPathology and Forensic Medicinechemistry.chemical_compoundFibrosisInternal medicineAtrial FibrillationmedicineBasic Helix-Loop-Helix Transcription FactorsHumansSinus rhythmAtrial AppendageHypoxiaMicrovesselAgedCell NucleusNeovascularization PathologicMicrocirculationMyocardiumAtrial fibrillationGeneral MedicineHypoxia (medical)Middle Agedmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitCoronary VesselsFibrosisUp-RegulationVascular endothelial growth factorEndocrinologychemistryCardiologyFemalemedicine.symptomCardiology and Cardiovascular MedicineBiomarkersCardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
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Induction of trefoil factor (TFF)1, TFF2 and TFF3 by hypoxia is mediated by hypoxia inducible factor-1: implications for gastric mucosal healing

2008

Background and purpose:  Mucosal microcirculation is compromised during gastric damage induced by non-steroidal anti-inflammatory drugs, such as aspirin. Consequently, oxygen supply to epithelial cells is decreased. The trefoil factor (TFF) peptides are involved in mechanisms of defence and repair in the gastrointestinal tract but their regulation at sites of gastric injury is unknown. Experimental approach:  Hypoxia and expression of TFF genes and peptides were measured in the damaged stomach of aspirin-treated rats. In a human gastric cell line (AGS cells), the effects of hypoxia and of hypoxia inducible factor (HIF)-1 (through transient transfection of HIF-1α siRNA or over-expression of …

Malemedicine.medical_specialtyTFF peptidesBiologyCell LineRats Sprague-DawleyInternal medicineGene expressionmedicineGastric mucosaAnimalsHumansRNA MessengereducationPharmacologyeducation.field_of_studyAspirinhypoxiaStomachAnti-Inflammatory Agents Non-SteroidalHIF-1Trefoil factor 2Epithelial CellsTransfectionHypoxia (medical)TFF genesepithelial cellsCell HypoxiaRatsUp-RegulationEndocrinologymedicine.anatomical_structureHypoxia-inducible factorsCell cultureGastric Mucosagastric damageCancer researchHypoxia-Inducible Factor 1Trefoil Factor-2medicine.symptomPeptidesResearch Paper
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The CO-releasing molecule CORM-2 is a novel regulator of the inflammatory process in osteoarthritic chondrocytes

2008

Previous work has shown that the CO-releasing molecule CORM-2 protects against cartilage degradation. The aim of this study was to examine whether CORM-2 can control the production of inflammatory mediators in osteoarthritic chondrocytes and determine the mechanisms involved.Primary cultures of chondrocytes from OA patients were stimulated with IL-1beta. The production of reactive oxygen species, nitrite, PGE(2), TNF-alpha and IL-1 receptor antagonist (IL-1Ra) were measured in the presence or absence of CORM-2. The expression of nitric oxide synthase-2 (NOS-2), cyclo-oxygenase-2 (COX-2) and microsomal PG E synthase-1 (mPGES-1) was followed by western blot and real-time PCR. Activation of nu…

Malemedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IINitric Oxidemedicine.disease_causeDinoprostoneChondrocyteNitric oxidechemistry.chemical_compoundChondrocytesRheumatologyWestern blotInternal medicineOsteoarthritisOrganometallic CompoundsmedicineHumansPharmacology (medical)Cells CulturedAgedProstaglandin-E SynthasesAged 80 and overchemistry.chemical_classificationReactive oxygen speciesDose-Response Relationship Drugmedicine.diagnostic_testTumor Necrosis Factor-alphabusiness.industryNF-kappa BHypoxia-Inducible Factor 1 alpha SubunitReceptor antagonistMolecular biologyIntramolecular OxidoreductasesInterleukin 1 Receptor Antagonist ProteinEndocrinologymedicine.anatomical_structureCytokinechemistryCyclooxygenase 2PhosphorylationFemaleReactive Oxygen SpeciesbusinessOxidative stressRheumatology
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Co-administration of human MSC overexpressing HIF-1α increases human CD34+ cell engraftment in vivo

2021

Abstract Background Poor graft function or graft failure after allogeneic stem cell transplantation is an unmet medical need, in which mesenchymal stromal cells (MSC) constitute an attractive potential therapeutic approach. Hypoxia-inducible factor-1α (HIF-1α) overexpression in MSC (HIF-MSC) potentiates the angiogenic and immunomodulatory properties of these cells, so we hypothesized that co-transplantation of MSC-HIF with CD34+ human cord blood cells would also enhance hematopoietic stem cell engraftment and function both in vitro and in vivo. Methods Human MSC were obtained from dental pulp. Lentiviral overexpression of HIF-1α was performed transducing cells with pWPI-green fluorescent pr…

Medicine (General)Mesenchymal stromal cellsMedicine (miscellaneous)HIF-1αAntigens CD34Trasplantació d'òrgans teixits etc.Mice SCIDQD415-436Biochemistry Genetics and Molecular Biology (miscellaneous)BiochemistryMiceR5-920Mice Inbred NODPoor graft functionAnimalsHumansResearchHematopoietic Stem Cell TransplantationStem cell transplantationEngraftmentMesenchymal Stem CellsCell BiologyFetal BloodHypoxia-Inducible Factor 1 alpha SubunitMolecular MedicineGraft failureCèl·lules mareHematopoietic stem cellsStem Cell Research & Therapy
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Identification of a novel recurrent 1q42.2-1qter deletion in high risk MYCN single copy 11q deleted neuroblastomas

2012

Neuroblastoma is an aggressive embryonal tumor that accounts for similar to 15% of childhood cancer deaths. Hitherto, despite the availability of comprehensive genomic data on DNA copy number changes in neuroblastoma, relatively little is known about the genes driving neuroblastoma tumorigenesis. In this study, high resolution array comparative genome hybridization (CGH) was performed on 188 primary neuroblastoma tumors and 33 neuroblastoma cell lines to search for previously undetected recurrent DNA copy number gains and losses. A new recurrent distal chromosome 1q deletion (del(1)(q42.2qter)) was detected in seven cases. Further analysis of available array CGH datasets revealed 13 additio…

Neuroblastoma/geneticsCancer ResearchProcollagen-Proline DioxygenaseMedizinGene Dosagecomparative genomic hybridizationBiologymedicine.disease_causeGene dosageN-Myc Proto-Oncogene ProteinFumarate HydrataseHypoxia-Inducible Factor-Proline DioxygenasesNeuroblastomaProcollagen-Proline Dioxygenase/geneticsCell Line TumorNeuroblastomamedicineHumansFumarate Hydratase/geneticsGeneOncogene ProteinsGeneticsN-Myc Proto-Oncogene ProteinChromosomes Human Pair 11BreakpointNuclear ProteinsChromosomemedicine.diseaseOncogene Proteins/geneticsNuclear Proteins/geneticsOncologyChromosome DeletionCarcinogenesisComparative genomic hybridization
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