Search results for "Up-Regulation"

showing 10 items of 455 documents

Obesity causes PGC‐1α deficiency in the pancreas leading to marked IL‐6 upregulation via NF‐κB in acute pancreatitis

2019

Obesity is associated with local and systemic complications in acute pancreatitis. PPARγ coactivator 1α (PGC-1α) is a transcriptional coactivator and master regulator of mitochondrial biogenesis that exhibits dysregulation in obese subjects. Our aims were: (1) to study PGC-1α levels in pancreas from lean or obese rats and mice with acute pancreatitis; and (2) to determine the role of PGC-1α in the inflammatory response during acute pancreatitis elucidating the signaling pathways regulated by PGC-1α. Lean and obese Zucker rats and lean and obese C57BL6 mice were used first; subsequently, wild-type and PGC-1α knockout (KO) mice with cerulein-induced pancreatitis were used to assess the inflam…

MaleTaurocholic Acid0301 basic medicinemedicine.medical_specialtyPGC-1αPathology and Forensic Medicine03 medical and health sciencesDownregulation and upregulationInternal medicineAnimalsMedicineObesityPhosphorylationInterleukin 6PancreasCeruletideMice KnockoutIL-6biologyp65Interleukin-6business.industryNF-kappa BTranscription Factor RelAmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRats ZuckerUp-Regulation3. Good healthMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologymedicine.anatomical_structureMitochondrial biogenesisPancreatitisbiology.proteinPancreatitisAcute pancreatitisPPARGC1AbusinessPancreasCeruletideSignal TransductionThe Journal of Pathology
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Glutamate cysteine ligase up-regulation fails in necrotizing pancreatitis

2007

Glutathione depletion is a key factor in the development of acute pancreatitis. Our aim was to study the regulation of glutamate cysteine ligase, the rate-limiting enzyme in glutathione synthesis, in edematous or necrotizing pancreatitis in rats. Glutathione levels were kept low in necrotizing pancreatitis for several hours, with no increase in protein or mRNA levels of glutamate cysteine ligase subunits, despite binding of RNA polymerase II to their promoters and coding regions. The survival signal pathway mediated by ERK and c-MYC was activated, and c-MYC was recruited to the promoters. The failure in gene up-regulation seems to be due to a marked increase in cytosolic ribonuclease activi…

MaleTaurocholic AcidMAPK/ERK pathwayRNase PGlutamate-Cysteine LigaseRNA StabilityRNA polymerase IIBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundRibonucleasesTranscription (biology)Physiology (medical)medicineAnimalsEdemaRNA MessengerRibonucleaseRats WistarbiologyPancreatitis Acute NecrotizingNF-κBGlutathionemedicine.diseaseGlutathioneMolecular biologyRatsUp-RegulationPancreatitischemistrybiology.proteinPancreatitisRNA Polymerase IICeruletideTranscription FactorsFree Radical Biology and Medicine
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Thyroid hormone induction of the adrenoleukodystrophy-related gene (ABCD2).

2003

X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VLCFA) beta-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3'-tri-iodothyronine (T3) receptor (TRbeta) as a heterodimer and mediating T3 responsiveness of ABCD2 in its promoter conte…

MaleThyroid HormonesReceptors Retinoic AcidGene ExpressionATP-binding cassette transporterRetinoid X receptorRats Sprague-DawleyMiceABCD3Gene expressionABCD2medicineAnimalsHumansReceptorAdrenoleukodystrophyPromoter Regions GeneticGeneCells CulturedRepetitive Sequences Nucleic AcidPharmacologyChemokine CCL22Mice KnockoutReceptors Thyroid Hormonebiologymedicine.diseaseCell biologyRatsUp-RegulationOligodendrogliaRetinoid X ReceptorsLiverAstrocytesChemokines CCbiology.proteinCancer researchMolecular MedicineTriiodothyronineAdrenoleukodystrophyChemokine CCL17Transcription FactorsMolecular pharmacology
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High serum uric acid levels increase the risk of metabolic syndrome in elderly women: The PRO.V.A study

2015

Background and aims: Serum uric acid (SUA) is the end-product of purine metabolism in humans, and its levels often increase in subjects with metabolic syndrome (MetS). Despite several studies demonstrating a relationship between increased SUA levels and the prevalence of MetS, prospective data on SUA as a predictor of the incidence of MetS in the elderly are limited. Our aim was to conduct a prospective study on the association between SUA concentrations and the onset of MetS in an elderly Italian cohort. Methods and results: This is a cohort study (Progetto Veneto Anziani Pro.V.A.) involving community-dwelling subjects aged ≥65 years and followed up for a mean 4.4 years. We included 1128 p…

MaleTime FactorsEndocrinology Diabetes and MetabolismMedicine (miscellaneous)030204 cardiovascular system & hematologychemistry.chemical_compoundEndocrinology0302 clinical medicineElderlyLongitudinal StudiesProspective StudiesProspective cohort studyAged 80 and overMetabolic SyndromeCohort study; Community-dwelling adults; Elderly; Metabolic syndrome X; Uric acid; Medicine (miscellaneous); Nutrition and Dietetics; Endocrinology Diabetes and Metabolism; Cardiology and Cardiovascular MedicineNutrition and DieteticsIncidence (epidemiology)IncidenceAge FactorsUp-RegulationDiabetes and MetabolismItalyCohortFemaleCardiology and Cardiovascular MedicineCommunity-dwelling adultCohort studyCohort studymedicine.medical_specialtyNational Health and Nutrition Examination Survey030209 endocrinology & metabolismHyperuricemiaRisk Assessment03 medical and health sciencesSex FactorsMetabolic syndrome XInternal medicinemedicineHumansAgedProportional Hazards Modelsbusiness.industrymedicine.diseaseCommunity-dwelling adultsEndocrinologyLogistic ModelschemistryLinear ModelsUric acidMetabolic syndromebusinessBody mass indexUric acidBiomarkersFollow-Up Studies
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Sex-dependent changes in the pulmonary vasoconstriction potential of newborn rats following short-term oxygen exposure

2012

Chronic exposure to supplemental oxygen (O(2)) induces lung damage and mortality in a sex-dependent manner. The effect of short-term hyperoxia on the newborn pulmonary vasculature is unknown but is, however, of clinical significance in the neonatal resuscitation context. We hypothesize that short-term hyperoxia has a sex-dependent effect on the pulmonary vasculature.Following 1-h 100% O(2) exposure, the pulmonary arteries and lung tissues of newborn rats were evaluated.Superoxide dismutase 3 (SOD3) expression in female pups' lungs was increased as compared with that in the lungs of male pups. As compared with air-treated pups, the response of male pups to thromboxane was increased by O(2), …

MaleTime FactorsHypertension PulmonaryHyperoxiaPulmonary ArteryRats Sprague-DawleySex FactorsSuperoxidesPeroxynitrous AcidHypoxic pulmonary vasoconstrictionAnimalsVasoconstrictor AgentsMedicineFamilial Primary Pulmonary Hypertensionskin and connective tissue diseasesOXYGEN EXPOSURELungrho-Associated KinasesDose-Response Relationship DrugSuperoxide Dismutasebusiness.industryFree Radical ScavengersHydrogen PeroxideRatsUp-RegulationEnzyme ActivationDisease Models AnimalOxidative StressAnimals NewbornVasoconstrictionAnesthesiaPediatrics Perinatology and Child HealthFemalesense organsbusinessPediatric Research
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Chronic lithium salt treatment reduces CRE/CREB-directed gene transcription and reverses its upregulation by chronic psychosocial stress in transgeni…

2007

The molecular mechanism of action of the mood stabilizer lithium is assumed to involve changes in gene expression leading to neuronal adaptation. The transcription factor CREB (cAMP-responsive element binding protein) regulates the expression of many genes and has been implicated in important brain functions and the action of psychogenic agents. We here investigated the effect of lithium on cAMP-responsive element (CRE)/CREB-mediated gene transcription in the brain, using transgenic reporter mice that express the luciferase reporter gene under the control of four copies of the rat somatostatin gene promoter CRE. Chronic (21 days) but not acute (24 h) treatment with lithium (7.5 mmol/kg) sig…

MaleTranscriptional ActivationBipolar DisorderTransgeneDown-RegulationMice TransgenicCREBDrug Administration Schedule03 medical and health sciencesGlycogen Synthase Kinase 3Mice0302 clinical medicineGSK-3Transcription (biology)Antimanic AgentsGenes ReporterGene expressionAnimalsPhosphorylationProtein kinase ACyclic AMP Response Element-Binding ProteinSocial BehaviorTranscription factor030304 developmental biologyPharmacology0303 health sciencesReporter genebiologyBehavior AnimalBrainMolecular biologyUp-RegulationPsychiatry and Mental healthDisease Models AnimalGene Expression RegulationChronic Diseasebiology.proteinLithium Compounds030217 neurology & neurosurgeryStress PsychologicalAdenylyl CyclasesSignal TransductionNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
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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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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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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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Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis

2004

Rat adjuvant arthritis is an experimental model widely used to evaluate etiopathogenetic mechanisms in chronic inflammation. We have examined the participation of heme oxygenase-1 (HO-1) in this experimental arthritis. In this study, an increased nitric oxide (NO) production in the paw preceded the upregulation of HO-1, whereas selective inhibition of inducible NO synthase (iNOS) after the onset of arthritis decreased HO-1 expression, suggesting that the induction of this enzyme may depend on NO produced by iNOS. Therapeutic administration of the HO-1 inhibitor tin protoporphyrin IX was able to control the symptoms of arthritis. This agent significantly decreased leukocyte infiltration, hyp…

MaleVascular Endothelial Growth Factor AOsteolysisAngiogenesisNitric Oxide Synthase Type IIProtoporphyrinsArthritisInflammationPharmacologyNitric OxidePathology and Forensic MedicineSynovitismedicineAnimalsEnzyme InhibitorsMolecular BiologyHeat-Shock ProteinsbiologyTumor Necrosis Factor-alphabusiness.industryLysineCell Biologymedicine.diseaseArthritis ExperimentalHindlimbRatsUp-RegulationNitric oxide synthaseHeme oxygenaseDisease Models AnimalCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesRats Inbred LewHeme Oxygenase (Decyclizing)ImmunologyOxygenasesbiology.proteinNitric Oxide Synthasemedicine.symptomVascular endothelial growth factor productionbusinessLaboratory Investigation
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