Search results for " Type II"

showing 10 items of 542 documents

Non-cross-linked collagen type I/III materials enhance cell proliferation: in vitro and in vivo evidence

2014

Objective: To analyze Mucograft®(MG), a recently introduced collagen matrix, in vitro and in vivo, and compare it with BioGide®(BG), a well-established collagen membrane, as control. Material and Methods: A detailed analysis of the materials surface and ultra-structure was performed. Cellular growth patterns and proliferation rates of human fibroblasts on MG and BG were analyzed in vitro. In addition, the early tissue reaction of CD-1 mouse to these materials was analyzed by means of histological and histomorphometrical analysis. Results: MG showed a three-fold higher thickness both in dry and wet conditions, when compared to BG. The spongy surface of BG significantly differed from that of …

Time FactorsCell SurvivalSurface PropertiesCellBiocompatible MaterialsMatrix (biology)BiologyPeripheral blood mononuclear cellCollagen Type IIIMiceRandom AllocationCollagen type IIn vivoMaterials TestingmedicineAnimalsHumansddc:610Bone regenerationGeneral DentistryCells CulturedCell ProliferationGuided tissue regenerationCell growthReproducibility of ResultsAnatomyOriginal ArticlesFibroblastsCollagen type IIIMolecular biologyImmunohistochemistryIn vitroBone regenerationlcsh:RK1-715medicine.anatomical_structurelcsh:DentistryFemaleCollagenJournal of Applied Oral Science
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REDUCTION OF NILUTAMIDE BY NO SYNTHASES : IMPLICATIONS FOR THE ADVERSE EFFECTS OF THIS NITROAROMATIC ANTIANDROGEN DRUG

2003

Nitric oxide synthases (NOSs) are flavohemeproteins that catalyze the oxidation of l-arginine to l-citrulline with formation of the widespread signal molecule NO. Beside their fundamental role in NO biosynthesis, these enzymes are also involved in the formation of reactive oxygen species and in the interactions with some xenobiotic compounds. Nilutamide is a nonsteroidal antiandrogen that behaves as a competitive antagonist of the androgen receptors and is proposed in the treatment of metastatic prostatic carcinoma. However, therapeutic effects of nilutamide are overshadowed by the occurrence of several adverse reactions mediated by toxic mechanism(s), which remain(s) poorly investigated. H…

Time FactorsFree RadicalsNitric Oxide Synthase Type IIImedicine.drug_class[CHIM.THER] Chemical Sciences/Medicinal ChemistryNitric Oxide Synthase Type IINitric Oxide Synthase Type I[CHIM.THER]Chemical Sciences/Medicinal ChemistryToxicologyAntiandrogenImidazolidinesNitric oxide03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineHydroxylaminemedicineAnimalsAnaerobiosisAmines030304 developmental biologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesElectron Spin Resonance SpectroscopyImidazolesAndrogen AntagonistsGeneral MedicineRecombinant Proteins3. Good healthRatsAndrogen receptorEnzymechemistryBiochemistryCompetitive antagonist030220 oncology & carcinogenesisNilutamideCattleNitric Oxide SynthaseOxidation-ReductionNADPmedicine.drug
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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
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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
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Beclomethasone dipropionate and formoterol reduce oxidative/nitrosative stress generated by cigarette smoke extracts and IL-17A in human bronchial ep…

2013

Interleukin-17A (IL-17A), cigarette smoke and oxidative/nitrosative stress are involved in inflammatory airway diseases, and the mechanisms behind these processes are still poorly understood. We investigated whether recombinant human IL-17A (rhIL-17A), in combination with cigarette smoke extracts (CSE), increases the levels of inducibile nitric oxide synthase (iNOS), reactive oxygen species, nitrotyrosine (NT) and the activation of signal transducer and activator of transcription 1 (STAT-1) in normal human bronchial epithelial cells (16HBE). The effect of beclomethasone dipropionate (BDP), formoterol and their combination was also evaluated. We demonstrated that rhIL-17A or CSE alone increa…

Transcription GeneticNitric Oxide Synthase Type IIBronchiOxidative phosphorylationPharmacologyGene Expression Regulation EnzymologicCell Linechemistry.chemical_compoundFormoterol FumarateSmokeNitrilesmedicineButadienesGene silencingHumansGene SilencingPromoter Regions GeneticPharmacologychemistry.chemical_classificationReactive oxygen speciesbiologyNitrotyrosineInterleukin-17BeclomethasoneEpithelial CellsTobacco ProductsReactive Nitrogen SpeciesNitric oxide synthaseOxidative StressSTAT1 Transcription FactorchemistryEthanolaminesImmunologySTAT proteinbiology.proteinPhosphorylationFormoterolBiomarkersmedicine.drugEuropean journal of pharmacology
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Role of SIRT1 and FOXO factors in eNOS transcriptional activation by resveratrol.

2013

Many of the cardiovascular protective effects of resveratrol are attributable to an enhanced production of nitric oxide (NO) by the endothelial NO synthase (eNOS). Resveratrol has been shown to enhance eNOS gene expression as well as eNOS enzymatic activity. The aim of the present study was to analyze the molecular mechanisms of eNOS transcriptional activation by resveratrol. Treatment of human EA.hy 926 endothelial cells with resveratrol led to a concentration-dependent upregulation of eNOS expression. In luciferase reporter gene assay, resveratrol enhanced the activity of human eNOS promoter fragments (3500, 1600, 633 and 263bp in length, respectively), indicating that the proximal promot…

Transcriptional ActivationCancer Researchendocrine system diseasesNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryFOXO1ResveratrolBiochemistryCell LineTransactivationchemistry.chemical_compoundSirtuin 1EnosStilbenesHumansRNA Small Interferingskin and connective tissue diseasesPromoter Regions GeneticTranscription factorGene knockdownAnalysis of VariancebiologySirtuin 1Chemistryorganic chemicalsfood and beveragesForkhead Transcription Factorsbiology.organism_classificationMolecular biologyUp-RegulationNitric oxide synthaseResveratrolGene Knockdown Techniquesbiology.proteinhormones hormone substitutes and hormone antagonistsNitric oxide : biology and chemistry
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Dual effect of ceramide on human endothelial cells: induction of oxidative stress and transcriptional upregulation of endothelial nitric oxide syntha…

2002

Background— Generation of the second-messenger molecule ceramide by stimulated sphingomyelinase activity has been implicated in the inflammatory processes contributing to the pathogenesis of atherosclerosis. However, reports of stimulatory effects of ceramide on endothelial NO production in animal models suggest antiatherosclerotic effects of the molecule. Therefore, we investigated long-term effects of ceramide on NO generation in human endothelial cells. Methods and Results— In human umbilical vein endothelial cells (HUVECs) and in HUVEC-derived EA.hy 926 endothelial cells, C6-ceramide ( N -hexanoyl- d -erythro-sphingosine) reduced the generation of bioactive NO (RFL-6 reporter-cell assa…

Transcriptional ActivationCeramideNitric Oxide Synthase Type IIIRNA StabilityBiologyCeramidesNitric OxideUmbilical veinCell Linechemistry.chemical_compoundDownregulation and upregulationEnosPhysiology (medical)Phosphoprotein PhosphatasesHumansEnzyme InhibitorsPromoter Regions GeneticCells CulturedDose-Response Relationship DrugLipid signalingbiology.organism_classificationCell biologyUp-RegulationNitric oxide synthaseEndothelial stem cellKineticsOxidative StressSphingomyelin PhosphodiesteraseBiochemistrychemistrybiology.proteinEndothelium VascularSignal transductionNitric Oxide SynthaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesCirculation
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Histamine Upregulates Gene Expression of Endothelial Nitric Oxide Synthase in Human Vascular Endothelial Cells

2003

Background— Histamine has a short-term, transient, stimulating effect on endothelial nitric oxide synthase (eNOS) activity; however, long-term effects on eNOS have not been described yet. In addition, the vascular effect of histamine seems to depend critically on eNOS functionality. Therefore, we studied the effects of histamine on eNOS gene expression and function. Methods and Results— In human umbilical vein endothelial cells (HUVECs) and HUVEC-derived EA.hy 926 cells, histamine upregulated eNOS mRNA (RNase protection assay) and protein (electron microscopic immunocytochemistry) expression. The upregulation of eNOS could be prevented by mepyramine, a selective antagonist at the H 1 recep…

Transcriptional Activationmedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumHistamine H1 receptorNitric OxideCell LineNitric oxidechemistry.chemical_compoundEnosPhysiology (medical)Internal medicinemedicineHumansRNA MessengerReceptors Histamine H1Enzyme InhibitorsPromoter Regions GeneticProtein Kinase InhibitorsCells CulturedDose-Response Relationship DrugbiologyNitric Oxide Synthase Type IIIbiology.organism_classificationMolecular biologyUp-RegulationNitric oxide synthaseKineticsOxidative StressEndocrinologymedicine.anatomical_structurechemistryEnzyme InductionCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinEndothelium VascularNitric Oxide SynthaseHistamine H3 receptorCalcium-Calmodulin-Dependent Protein Kinase Type 2Reactive Oxygen SpeciesCardiology and Cardiovascular MedicineHistamineHistamineCirculation
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Human inducible nitric oxide synthase (iNOS) expression depends on chromosome region maintenance 1 (CRM1)- and eukaryotic translation initiation fact…

2012

Human inducible nitric oxide synthase (iNOS) is regulated on the expressional level mostly by post-transcriptional mechanisms modulating the mRNA stability. Another important step in the control of eukaryotic gene expression is the nucleocytoplasmic mRNA transport. Most cellular mRNAs are exported via the TAP/Nxt complex of proteins. However, some mRNAs are transported by a different mechanism involving the nuclear export receptor CRM1. Treatment of DLD-1 cells with the CRM1 inhibitor leptomycin B (LMB) or anti-CRM1 siRNAs reduced cytokine-induced iNOS expression. We could demonstrate that the iNOS mRNA is exported from the nucleus in a CRM1-dependent manner. Since CRM1 itself does not poss…

Untranslated regionCancer ResearchPhysiologyClinical BiochemistryActive Transport Cell NucleusNitric Oxide Synthase Type IIReceptors Cytoplasmic and NuclearKaryopherinsBiologyenvironment and public healthBiochemistryRNA TransportEukaryotic translationCell Line TumorRibavirinGene expressionP-bodiesHumansMRNA transportRNA MessengerLuciferasesNuclear export signalAnalysis of VarianceMessenger RNAfungiEIF4EMolecular biologyEukaryotic Initiation Factor-4Elipids (amino acids peptides and proteins)Nitric Oxide
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Post-transcriptional regulation of the human inducible nitric oxide synthase (iNOS) expression by the cytosolic poly(A)-binding protein (PABP).

2012

Affinity purification using the 3'-untranslated region (3'-UTR) of the human inducible nitric oxide synthase (iNOS) mRNA identified the cytosolic poly(A)-binding protein (PABP) as a protein interacting with the human iNOS 3'-UTR. Downregulation of PABP expression by RNA interference resulted in a marked reduction of cytokine-induced iNOS mRNA expression without changes in the expression of mRNAs coding for the major subunit of the RNA polymerase II (Pol 2A) or β2-microglobuline (β2M). Along with the mRNA also iNOS protein expression was reduced by siPABP-treatment, whereas in the same cells protein expression of STAT-1α, NF-κB p65, or GAPDH was not altered. Reporter gene analyses showed no …

Untranslated regionCancer ResearchSmall interfering RNAFive prime untranslated regionPhysiologyClinical BiochemistryDown-RegulationNitric Oxide Synthase Type IIBiologyBiochemistryPoly(A)-Binding ProteinsCell Line TumorPoly(A)-binding proteinHumansRNA MessengerRNA Processing Post-TranscriptionalPost-transcriptional regulation3' Untranslated RegionsAU-rich elementMessenger RNABinding SitesThree prime untranslated regionMolecular biologyMutationbiology.proteinCytokinesNitric oxide : biology and chemistry
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