Search results for "Up-Regulation"

showing 10 items of 455 documents

Type-II transmembrane prolyl dipeptidases and matrix metalloproteinases in membrane vesicles of active endothelial cells.

2006

Conclusions: Endothelia cells in sparse culture are migratory and increase the production of gelatinases of serine- and metallo-classes in membrane vesicles. Collectively, proteases associated with membrane vesicles degrade extracellular matrix components including type-I and type-IV collagens, laminin and fibronectin. Inhibitor studies suggest the existence of small gelatinases that were derived from these serine- and metallo-proteases. Thus, further studies are warranted to demonstrate the cooperative action of metallo- and serine proteases on cell surfaces and in extracellular vesicles during endothelial cell migration in 3D collagenous matrices, and potential proteolytic activation mech…

TUMOR-CELLSCell MembraneBREAST-CARCINOMA CELLSEndothelial CellsUP-REGULATIONANGIOGENESISMatrix MetalloproteinasesExtracellular MatrixACTIVATIONEnzyme ActivationNEUROPEPTIDE-YCell MovementSEPRASESettore BIO/10 - BiochimicaMETASTASISPEPTIDASE-IVHumansDipeptidyl-Peptidases and Tripeptidyl-PeptidasesINTEGRINCells CulturedAdvances in experimental medicine and biology
researchProduct

Worldwide burden of LDL cholesterol: Implications in cardiovascular disease

2020

Abstract Background and aim an increased value of low-density lipoprotein cholesterol (LDL-C) is now universally considered a major cardiovascular disease (CVD) risk factor. LDL-C is included in the vast majority of worldwide cardiovascular risk prediction algorithms, as well as in the guidelines for cardiovascular risk prevention. We aimed to provide an overview of the worldwide adverse healthcare impact of low-density lipoprotein cholesterol (LDL-C). Methods and results Data on the epidemiologic burden of LDL-C >1.3 mmol/L were retrieved from Global Health Data Exchange (GHDx) registry. The current burden is 94.92 million disability-adjusted life years (DALYs), with an exponential increas…

Time FactorsDatabases FactualHealth StatusEndocrinology Diabetes and MetabolismMedicine (miscellaneous)030209 endocrinology & metabolismDisease030204 cardiovascular system & hematologyGlobal HealthRisk Assessment03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRisk FactorsEnvironmental healthHealth careGlobal healthHumansMedicineRegistriesRisk factorEpidemicsAtherosclerosis; Cardiovascular disease; Cholesterol; Low-density lipoproteinsDyslipidemiasLdl cholesterolNutrition and Dieteticsbusiness.industryCholesterolCholesterol LDLAtherosclerosisCardiovascular diseaseUp-RegulationPrediction algorithmsCholesterolchemistryCardiovascular DiseasesLow-density lipoproteinslipids (amino acids peptides and proteins)Risk preventionQuality-Adjusted Life YearsCardiology and Cardiovascular MedicinebusinessBiomarkersNutrition, Metabolism and Cardiovascular Diseases
researchProduct

The aryl hydrocarbon receptor modulates acute and late mast cell responses.

2012

Abstract The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activity is modulated by xenobiotics as well as physiological ligands. These compounds may modulate inflammatory responses and contribute to the rising prevalence of allergic diseases observed in industrialized countries. Mast cells (MCs), located within tissues at the boundary of the external environment, represent a potential target of AhR ligands. In this study, we report that murine and human MCs constitutively express AhR, and its activation by the high-affinity ligand 6-formylindolo[3,2-b]carbazole (FICZ) determines a boost in degranulation. On the contrary, repeated exposure to FICZ inhibits…

Time FactorsInbred C57BLLigandsCell DegranulationPathogenesischemistry.chemical_compoundMiceAnaphylaxiReceptorsMast CellImmunology and AllergyMast CellsReceptorMice KnockoutbiologyInterleukin-17DegranulationMast cellUp-RegulationImmunology Mast Cell Aryl Receptormedicine.anatomical_structureAryl HydrocarbonBone Marrow Celldeficiency/metabolism/physiologyIgEmedicine.symptomimmunology/metabolism/pathologyHistamineHumanReceptorTime FactorKnockoutImmunologyDown-RegulationLigandInflammationBone Marrow CellsSettore MED/08 - Anatomia PatologicaCell LinebiosynthesiAnaphylaxis; immunology/metabolism/pathology Animals Bone Marrow Cells; immunology/metabolism/pathology Cell Degranulation; genetics/immunology Cell Line Down-Regulation; genetics/immunology Humans Interleukin-17; biosynthesis Interleukin-6; biosynthesis Ligands Mast Cells; immunology/metabolism/pathology Mice Mice; Inbred C57BL Mice; Knockout Receptors; Aryl Hydrocarbon; deficiency/metabolism/physiology Receptors; IgE; physiology Time Factors Up-Regulation; genetics/immunologymedicineAnimalsHumansTranscription factorAnaphylaxisAnimalInterleukin-6Receptors IgEAryl hydrocarbon receptorgenetics/immunologyMice Inbred C57BLMAST CELL; ARYL HYDROCARBON RECEPTORchemistryReceptors Aryl HydrocarbonImmunologyphysiologybiology.proteinbiosynthesisJournal of immunology (Baltimore, Md. : 1950)
researchProduct

Short‐term hypoxia promotes vascularization in co‐culture system consisting of primary human osteoblasts and outgrowth endothelial cells

2019

Prevascularization of tissue constructs before implantation has been developed as a novel and promising concept for successful implantation. Since hypoxia might induce angiogenesis, we have investigated the effects of hypoxic treatment on vascularization by using co-cultures of primary human osteoblasts (POBs) and outgrowth endothelial cells. Our results show that: (a) repeated short-term hypoxia (2% O2 for 8 hr), not long-term hypoxia (2% O2 for 24 hr), over 1 or 2 weeks, significantly enhances microvessel formation in co-cultures; (b) sustained hypoxia, not short-term or long-term hypoxia, causes cytotoxicity in mono- and co-cultures; (c) the expression of some angiogenic and inflammatory…

Time FactorsMaterials scienceCell SurvivalAngiogenesisProtein subunitmedicine.medical_treatment0206 medical engineeringBiomedical EngineeringNeovascularization Physiologic02 engineering and technologyBone tissueBiomaterialschemistry.chemical_compoundmedicineHumansRNA MessengerCytotoxicityMicrovesselCells CulturedOsteoblastsCell DeathGrowth factorMetals and AlloysEndothelial CellsHypoxia (medical)021001 nanoscience & nanotechnology020601 biomedical engineeringCell HypoxiaCoculture TechniquesUp-RegulationVascular endothelial growth factormedicine.anatomical_structurechemistryCeramics and CompositesCancer researchInflammation Mediatorsmedicine.symptom0210 nano-technologyJournal of Biomedical Materials Research Part A
researchProduct

Prunella vulgaris L. Upregulates eNOS Expression in Human Endothelial Cells

2010

The purported effects of "circulation-improving" herbs used in traditional Chinese medicine (TCM) show striking similarities with the vascular actions of nitric oxide (NO) produced by the endothelial NO synthase (eNOS). We have previously reported that Salviae miltiorrhizae radix and Zizyphi spinosae semen upregulate eNOS expression. In the present study, we studied the effect on eNOS gene expression of 15 Chinese herbs with potential effects on the vasculature, and identified Prunella vulgaris L. (PVL) (flowering spike) as a potent eNOS-upregulating agent. In EA.hy 926 cells, a cell line derived from human umbilical vein endothelial cells (HUVEC), an aqueous extract of PVL increased eNOS …

Time FactorsNitric Oxide Synthase Type IIIEndotheliumCell SurvivalBlotting WesternPrunella vulgarisCynarosidePharmacologyNitric OxideGene Expression Regulation EnzymologicCell LineNitric oxidechemistry.chemical_compoundUrsolic acidEnosmedicineHumansPrunellaRNA MessengerDose-Response Relationship DrugbiologyEndothelial CellsGeneral Medicinebiology.organism_classificationUp-RegulationNitric oxide synthasemedicine.anatomical_structureComplementary and alternative medicinechemistryChild Preschoolbiology.proteinLuteolinDrugs Chinese HerbalThe American Journal of Chinese Medicine
researchProduct

In human endothelial cells rapamycin causes mTORC2 inhibition and impairs cell viability and function.

2008

Aim Drug-eluting stents are widely used to prevent restenosis but are associated with late endothelial damage. To understand the basis for this effect, we have studied the consequences of a prolonged incubation with rapamycin on the viability and functions of endothelial cells. Methods and results Human umbilical vein or aorta endothelial cells were exposed to rapamycin in the absence or in the presence of tumour necrosis factor α (TNFα). After a 24 h-incubation, rapamycin (100 nM) caused a significant cell loss associated with the increase of both apoptosis and necrosis, as quantified by propidium iodide staining, caspase 3 activity, and lactate dehydrogenase release. Rapamycin also impair…

Time FactorsPhysiologyApoptosismTORC1Polymerase Chain Reactionchemistry.chemical_compoundCell MovementStress FibersMicroscopy ConfocalCaspase 3TOR Serine-Threonine KinasesNitric Oxide Synthase Type IIIRibosomal Protein S6 Kinases 70-kDaUp-RegulationEndothelial stem cellmedicine.anatomical_structureBiochemistryCardiology and Cardiovascular MedicineE-SelectinEndotheliumNitric Oxide Synthase Type IIICell SurvivalBlotting WesternEnzyme-Linked Immunosorbent AssayBiologyMechanistic Target of Rapamycin Complex 1Nitric OxideTacrolimusNecrosisTheophyllinePhysiology (medical)medicineHumansImmunoprecipitationViability assayPropidium iodideProtein kinase BAdaptor Proteins Signal TransducingSirolimusDose-Response Relationship DrugL-Lactate DehydrogenaseTumor Necrosis Factor-alphaEndothelial CellsProteinsCardiovascular AgentsRegulatory-Associated Protein of mTORMolecular biologyRapamycin-Insensitive Companion of mTOR ProteinchemistryMultiprotein ComplexesTOR Serine-Threonine KinasesCarrier ProteinsProtein KinasesTranscription FactorsCardiovascular research
researchProduct

Glucocorticoid receptor regulates organic cation transporter 1 (OCT1, SLC22A1) expression via HNF4α upregulation in primary human hepatocytes

2013

Abstract Background Organic cation transporter 1 (OCT1, SLC22A1) is a membrane transporter that is important for therapeutic effect of the antidiabetic drug metformin. Its liver-specific expression in hepatocytes is strongly controlled by hepatocyte nuclear factor-4α (HNF4α). HNF4α expression and transcriptional activity have been demonstrated to be augmented by glucocorticoid receptor (GR) in human hepatocytes and rodent livers. Methods It was examined whether GR activation indirectly induces OCT1 gene expression via HNF4α up-regulation in primary human hepatocytes.We also examined which other transcription factors are involved in OCT1 gene expression and whether they are regulated by dexa…

Time FactorsPrimary Cell CultureTransfectionDexamethasoneReceptors GlucocorticoidGlucocorticoid receptorTransduction GeneticEnhancer bindingCoactivatorGene expressionHumansRNA MessengerGlucocorticoidsTranscription factorPharmacologyRegulation of gene expressionChemistryCCAAT-Enhancer-Binding Protein-betaOrganic Cation Transporter 1Hep G2 CellsGeneral MedicineTransfectionPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMolecular biologyUp-RegulationHepatocyte Nuclear Factor 4Cell cultureHepatocytesTranscription FactorsPharmacological Reports
researchProduct

Insulin-like growth factor 1 differentially regulates estrogen receptor-dependent transcription at estrogen response element and AP-1 sites in breast…

2007

Cross-talk between insulin-like growth factor 1 (IGF-1) and estrogen receptor alpha (ER) regulates gene expression in breast cancer cells, but the underlying mechanisms remain unclear. Here, we studied how 17-beta-estradiol (E2) and IGF-1 affect ER transcriptional machinery in MCF-7 cells. E2 treatment stimulated ER loading on the estrogen response element (ERE) in the pS2 promoter and on the AP-1 motif in the cyclin D1 promoter. On ERE, similar amounts of liganded ER were found at 1-24-h time points, whereas on AP-1, ER binding fluctuated over time. At 1 h, liganded ER was recruited to ERE together with histone acetyltransferases SRC-1 and p300, ubiquitin ligase E6-AP, histone methyltransf…

Transcription GeneticActive Transport Cell NucleusEstrogen receptorBreast NeoplasmsLigandsResponse ElementsBiochemistryCyclin D1Cell Line TumorHumansCyclin D1RNA MessengerInsulin-Like Growth Factor IHistone H3 acetylationMolecular BiologyHormone response elementbiologyEstradiolTumor Suppressor ProteinsEstrogen Receptor alphaCell BiologyUbiquitin ligaseCell biologyUp-RegulationTranscription Factor AP-1Histone methyltransferasebiology.proteinCancer researchMdm2Trefoil Factor-1Estrogen receptor alphahormones hormone substitutes and hormone antagonistsThe Journal of biological chemistry
researchProduct

Indicaxanthin from

2018

Oxidized low-density lipoproteins (oxLDL) play a pivotal role in the etiopathogenesis of atherosclerosis through the activation of inflammatory signaling events eventually leading to endothelial dysfunction and senescence. In the present work, we investigated the effects of indicaxanthin, a bioavailable, redox-modulating phytochemical from Opuntia ficus indica fruits, with anti-inflammatory activity, against oxLDL-induced endothelial dysfunction. Human umbilical vein cord cells (HUVEC) were stimulated with human oxLDL, and the effects of indicaxanthin were evaluated in a range between 5 and 20 μM, consistent with its plasma level after a fruit meal (7 μM). Pretreatment with indicaxanthin si…

Transcription GeneticCell SurvivalPyridinesNF-kappa BOpuntiaHydrogen PeroxideReactive Nitrogen SpeciesThiobarbituric Acid Reactive SubstancesBetaxanthinsUp-RegulationLipoproteins LDLHuman Umbilical Vein Endothelial CellsHumansRNA MessengerReactive Oxygen SpeciesCell Adhesion MoleculesOxidation-ReductionATP Binding Cassette Transporter 1Research ArticleOxidative medicine and cellular longevity
researchProduct

Transcription of different exons 1 of the human neuronal nitric oxide synthase gene is dynamically regulated in a cell- and stimulus-specific manner.

2003

An extensive screening of the human neuronal nitric oxide synthase (nNOS) mRNAs in various human tissues and cell lines unraveled an extreme complexity in the transcription of this gene. Using 5'rapid amplification of cDNA ends (5'-RACE), ten different exons 1 (named 1a-1l) were identified. They were spliced in a cell-specific manner to a common exon 2, which bears the translational start site. Three first exons (1 d, 1g and 1f) were used predominantly for the transcription of the nNOS gene (146 out of 197 5'-RACE clones contained these exons). Exon 1 k was found alone, but in many instances was interposed between exons 1 b, 1d, 1g, 1 i or 1j and the common exon 2. In addition to the cell-s…

Transcription GeneticClinical BiochemistryMolecular Sequence DataNitric Oxide Synthase Type IBiologyBiochemistryGene Expression Regulation EnzymologicExonDownregulation and upregulationEpidermal growth factorTranscription (biology)Complementary DNATumor Cells CulturedHumansRNA MessengerCloning MolecularMolecular BiologyGeneMessenger RNABase SequenceExonsMolecular biologyUp-RegulationAlternative SplicingBucladesineCell cultureNitric Oxide SynthaseBiological chemistry
researchProduct