Search results for "down-regulation"

showing 10 items of 310 documents

Downregulation of intratumoral expression of miR-205, miR-200c and miR-125b in primary human cutaneous melanomas predicts shorter survival

2018

AbstractWhile only 15–25 percent of melanoma patients develop distant metastasis and die, this disease is still responsible for the majority of skin cancer-related deaths. The availability of adjuvant therapies makes the selection of high-risk patients essential. We evaluated the intratumoral expression of ten miRNAs in primary melanomas in relation to its ability to predict melanoma survival. To this end, we correlated miRNA expression in 132 cryopreserved primary and metastatic tumors with clinicopathological factors and clinical outcome. We found sequential downregulation of intratumoral expression of miR-125b, miR-182, miR-200c and miR-205 over the full spectrum of melanoma progression.…

Male0301 basic medicineSkin Neoplasmsmedicine.medical_treatmentlcsh:MedicineDown-RegulationDiseaseArticleMetastasisExtracellular matrix03 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementmicroRNABiomarkers TumorTumor Cells CulturedmedicineHumansNeoplasm Invasivenesslcsh:ScienceMelanomaAgedCell ProliferationMultidisciplinarybusiness.industryMelanomalcsh:RPrognosismedicine.diseaseIn vitroGene Expression Regulation NeoplasticSurvival RateMicroRNAs030104 developmental biology030220 oncology & carcinogenesisDisease ProgressionCancer researchlcsh:QFemalebusinessAdjuvantFollow-Up StudiesScientific Reports
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EGFR gene copy number decreases during anti-EGFR antibody therapy in colorectal cancer

2018

Epidermal growth factor receptor (EGFR) gene copy number (GCN) increase is associated with a favorable anti-EGFR antibody treatment response in RAS wild-type metastatic colorectal cancer. However, there are limited and comparative data regarding the EGFR GCN in primary colorectal cancer tumors and corresponding metastases or the effect of anti-EGFR antibody treatment on EGFR GCN in recurrent disease. In addition, little is known about the potential EGFR GCN changes during anti-EGFR therapy in comparison with other treatment regimens. EGFR GCN was analyzed by EGFR immunohistochemistry-guided silver in situ hybridization in primary and corresponding recurrent local or metastatic tumors from 8…

Male0301 basic medicineTime FactorsColorectal cancerBLOCKADEGene DosageCetuximabmedicine.disease_causeAntineoplastic Agents Immunological0302 clinical medicinePREDICTS RESPONSEMedicineHETEROGENEITYBENEFITCopy-number variationEpidermal growth factor receptorIn Situ Hybridization FluorescenceAged 80 and overbiologyPanitumumabvasta-aineetMiddle AgedImmunohistochemistry3. Good healthErbB ReceptorsGene Expression Regulation NeoplasticTreatment OutcomeRAS MUTATIONSChemotherapy Adjuvant030220 oncology & carcinogenesisFemaleKRASAntibodyColorectal NeoplasmsAdultgene copy numbermedicine.drug_classCETUXIMAB THERAPY3122 Cancerssilver in situ hybridizationDown-Regulationcolorectal cancerIn situ hybridizationAdenocarcinomaMonoclonal antibodyta3111Pathology and Forensic MedicineProto-Oncogene Proteins p21(ras)03 medical and health sciencesKRASHumansWILD-TYPEMETAANALYSISAgedRetrospective Studiessyöpähoidotbusiness.industrymedicine.diseaseta3122Blockadeperäsuolisyöpä030104 developmental biologymonoclonal antibodyMutationCancer researchbiology.protein3111 BiomedicineNeoplasm Recurrence Localbusinessepidermal growth factor receptorACQUIRED-RESISTANCEHuman Pathology
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Cigarette Smoking is Associated with Decreased Bone Gla-protein (BGP) Levels in Hemodialysis Patients

2018

Background: Bone Gamma-carboxyglutamic acid (Gla)-protein (BGP or osteocalcin) is a vitamin K-dependent protein involved in the regulation of bone mineralization. Smoking is a risk factor for osteoporosis. Methods: We carried out a secondary analysis of the Vitamin K Italian (VIKI) study to investigate the association between cigarette smoking and BGP levels in patients with end stage renal disease. Data were collected in 370 haemodialysis patients, 37% (136) smokers (or ex-smokers) and 63% (234) nonsmokers. Vascular calcifications and vertebral fractures (quantitative morphometry) were identified on spine radiographs. Results: Smokers had significantly lower BGP levels (152 vs. 204 μg/L, p…

Male0301 basic medicineVitaminmedicine.medical_specialtymedicine.medical_treatmentOsteocalcinPopulationOsteoporosisDown-RegulationboneGastroenterologyCigarette SmokingEnd stage renal disease03 medical and health scienceschemistry.chemical_compoundRenal DialysisRisk FactorsInternal medicineHumansMedicineRisk factorVascular CalcificationeducationAgedPharmacologyeducation.field_of_studySmokersbiologybusiness.industry030111 toxicologyBGPNon-SmokersMiddle Agedmedicine.diseasehaemodialysismokeItalychemistryOsteocalcinbiology.proteinKidney Failure ChronicSpinal FracturesFemaleHemodialysisCardiology and Cardiovascular MedicinebusinessBiomarkersOsteoporotic FracturesCalcificationCurrent Vascular Pharmacology
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Downregulation of miR-31 in Diabetic Nephropathy and its Relationship with Inflammation

2018

Background/Aims: There is a lack of reliable biological markers for the early diagnosis of diabetic nephropathy (DN) during type 2 diabetes. In this pilot study we aim to assess whether miR-31 levels are modulated by the presence of DN and whether the expression of this miRNA is related to leukocyte-endothelial interactions and inflammation. Methods: Thirty-one T2D patients were enrolled in this pilot study; 18 with no diabetic complications and 13 with diabetic nephropathy. 24 non-diabetic subjects and 13 T2D patients with retinopathy (absent of other complications) were included to test the specificity of miR-31. Following anthropometric and biochemical evaluation, serum miR-31 levels wer…

Male0301 basic medicinemedicine.medical_specialtyPhysiologyDown-RegulationInflammationType 2 diabeteslcsh:PhysiologyNephropathylcsh:BiochemistryDiabetic nephropathy03 medical and health sciences0302 clinical medicineInternal medicineCell AdhesionmedicineAlbuminuriaHumanslcsh:QD415-436Diabetic NephropathiesAgedInflammationlcsh:QP1-981Interleukin-6Tumor Necrosis Factor-alphabusiness.industryEndothelial CellsType 2 diabetesMiddle AgedIntercellular Adhesion Molecule-1medicine.diseaseNephropathymir-31MicroRNAs030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2030220 oncology & carcinogenesismiRNAsLeukocytes MononuclearBiomarker (medicine)Leukocyte-endothelial interactionFemaleMicroalbuminuriamedicine.symptombusinessBiomarkersRetinopathyCellular Physiology and Biochemistry
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Downregulation of PMCA2 increases the vulnerability of midbrain neurons to mitochondrial complex I inhibition

2013

Parkinson's disease is an age-associated disorder characterized by selective degeneration of dopaminergic neurons. The molecular mechanisms underlying the selective vulnerability of this subset of neurons are, however, not fully understood. Employing SH-SY5Y neuroblastoma cells and primary mesencephalic neurons, we here demonstrate a significant increase in cytosolic calcium after inhibition of mitochondrial complex I by means of MPP(+), which is a well-established environmental toxin-based in vitro model of Parkinson's disease. This increase in calcium is correlated with a downregulation of the neuron-specific plasma membrane Ca(2+)-ATPase isoform 2 (PMCA2). Interestingly, two other import…

Male1-Methyl-4-phenylpyridiniummedicine.medical_specialtySERCADown-Regulationchemistry.chemical_elementCalciumToxicologyCREBRats Sprague-DawleyPlasma Membrane Calcium-Transporting ATPaseschemistry.chemical_compoundDownregulation and upregulationMesencephalonCell Line TumorInternal medicinemedicineAnimalsHumansCyclic AMP Response Element-Binding ProteinNeuronsCalcium metabolismElectron Transport Complex IbiologyGeneral NeuroscienceMPTPNeurodegenerationmedicine.diseaseRatsEndocrinologychemistrybiology.proteinCalciumsense organsIntracellularNeuroToxicology
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Aging-induced Up-regulation of Nuclear Binding Activities of Oxidative Stress Responsive NF-kB Transcription Factor in Mouse Cardiac Muscle

1996

The accumulation of lipofuscin to cardiomyocytes is a classical parameter of aging and is believed to reflect oxidative stress. NF-kB transcription factor complex is one of the cellular sensors which responds to oxidative stress and regulates gene expression. Our purpose was to study whether aging affects the level and distribution of DNA binding activities of NF-kB transcription factors both in cardiac sarcoplasm and nuclear extracts. We used electrophoretic mobility shift assays (EMSA) to characterize the DNA binding activities of NF-kB and two other transcription factors. AP-1 and Sp-1, in the myocardium of 4 months and 24 months old male and female NMRI-mice. The protein levels of p50, …

MaleAgingP50Sp1 Transcription FactorSarcoplasmDown-RegulationTranscription factor complexBiologymedicine.disease_causeMiceNF-KappaB Inhibitor alphaGene expressionmedicineAnimalsMolecular BiologyTranscription factorCell NucleusMyocardiumNF-kappa BTranscription Factor RelACardiac muscleNF-kappa B p50 SubunitNF-kappa B p50 SubunitMolecular biologyUp-RegulationDNA-Binding ProteinsTranscription Factor AP-1Oxidative Stressmedicine.anatomical_structureFemaleI-kappa B ProteinsCardiology and Cardiovascular MedicineOxidative stressJournal of Molecular and Cellular Cardiology
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Haem oxygenase-1 down-regulates high mobility group box 1 and matrix metalloproteinases in osteoarthritic synoviocytes

2010

Objectives. Activation of osteoarthritic synoviocytes by pro-inflammatory cytokines results in the release of biochemical mediators such as MMPs and high mobility group box 1 (HMGB1). Extracellular HMGB1 can play an important role in joint diseases as a mediator of synovitis. We have shown previously that haem oxygenase-1 (HO-1) exerts protective effects during inflammatory responses. In this study, we have examined whether HO-1 induction would be an effective strategy to control MMP and HMGB1 production in osteoarthritic synoviocytes. Methods. Osteoarthritic synoviocytes were obtained by digestion with collagenase and cultured until third passage. HO-1 was induced by cobalt protoporphyrin …

MaleAnalysis of VarianceSmall interfering RNASynovial MembraneDown-RegulationTransfectionBiologyMatrix metalloproteinaseHMGB1COPPMolecular biologyMatrix MetalloproteinasesRheumatologyOsteoarthritisGene expressionbiology.proteinHumansGene silencingInterstitial collagenaseFemalePharmacology (medical)HMGB1 ProteinCells CulturedHeme Oxygenase-1AgedRheumatology
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Conditioned Media from Adipose-Tissue-Derived Mesenchymal Stem Cells Downregulate Degradative Mediators Induced by Interleukin-1β in Osteoarthritic C…

2013

Osteoarthritis (OA) is the most frequent joint disorder and an important cause of disability. Recent studies have shown the potential of adipose-tissue-derived mesenchymal stem cells (AD-MSC) for cartilage repair. We have investigated whether conditioned medium from AD-MSC (CM) may regulate in OA chondrocytes a number of key mediators involved in cartilage degeneration. CM enhanced type II collagen expression in OA chondrocytes while decreasing matrix metalloproteinase (MMP) activity in cell supernatants as well as the levels of MMP-3 and MMP-13 proteins and mRNA in OA chondrocytes stimulated with interleukin- (IL-) 1β. In addition, CM increased IL-10 levels and counteracted the stimulating…

MaleArticle Subjectmedicine.medical_treatmentImmunologyInterleukin-1betaType II collagenAdipose tissueDown-RegulationNitric OxideChondrocytesMatrix Metalloproteinase 13Osteoarthritislcsh:PathologymedicineHumansProstaglandin E2Interleukin 6Collagen Type IICells CulturedAgedbiologyChemistryInterleukin-6Tumor Necrosis Factor-alphaMesenchymal stem cellNF-kappa BInterleukinMesenchymal Stem CellsCell BiologyMiddle AgedCell biologyAdipose TissueCulture Media ConditionedImmunologybiology.proteinTumor necrosis factor alphaFemaleMatrix Metalloproteinase 3Inflammation Mediatorslcsh:RB1-214Prostaglandin Emedicine.drugResearch Article
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Inhibition of iNOS activity by 1400W decreases glutamate release and ameliorates stroke outcome after experimental ischemia

2005

Background and purpose. It has been shown that the reversed operation of glutamate transporters when ATP levels fall accounts for most glutamate release induced by severe cerebral ischemia. Nitric oxide (NO) is formed after ischemia and causes ATP depletion. Our purpose is to test if NO release from inducible NO synthase (iNOS) after stroke may cause a delayed glutamate release due to ATP depletion that might underlie progression of the ischemic infarct. We have studied the effect of the highly selective inhibitor of iNOS activity 1400W on brain ATP levels, extracellular glutamate, and stroke outcome after transient focal cerebral ischemia in rats. Methods. To induce focal ischemia, the mid…

MaleBenzylaminesAmino Acid Transport System X-AGIschemiaAmidinesInfarctionDown-RegulationGlutamic AcidNitric Oxide Synthase Type IIL-argininePharmacologyNeuroprotectionNitric oxidelcsh:RC321-571chemistry.chemical_compoundAdenosine TriphosphateWestern blotmedicine.arteryStroke outcomeMedicineAnimalscardiovascular diseasesEnzyme InhibitorsRats Wistarlcsh:Neurosciences. Biological psychiatry. Neuropsychiatrymedicine.diagnostic_testbusiness.industryGlutamate receptorBrainInfarction Middle Cerebral ArteryNitric oxideCerebral Infarctionmedicine.diseaseNeuroprotectionRatsATPStrokeDisease Models AnimalNeuroprotective AgentsTreatment OutcomeNeurologychemistryCytoprotectionIschemic Attack TransientAnesthesiaMiddle cerebral arteryNitric Oxide SynthaseGlutamatebusinessNeurobiology of Disease
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Trastuzumab therapy vs tetracycline controlled ERBB2 downregulation: influence on tumour development in an ERBB2-dependent mouse tumour model

2008

Trastuzumab (Herceptin) has improved therapy of breast cancer. Only patients overexpressing ERBB2 are treated with trastuzumab, whereas its use in tumours without ERBB2 expression is useless. This led to the concept that the subgroup of trastuzumab-sensitive tumours is ‘ERBB2-dependent', meaning that ERBB2 signalling is indispensable for growth of these tumours. We used a mouse model that allows anhydrotetracycline (ATc)-controlled downregulation of ERBB2 in tumour tissue. ERBB2 mRNA and protein expression were downregulated below detection limit leading to a macroscopically complete tumour remission within 14 days. Tumour remission was accompanied by a strong decrease in proliferation, a m…

MaleCancer ResearchReceptor ErbB-2AKT1AKT2ApoptosisMiceTrastuzumabPKBskin and connective tissue diseasesERBB2Mitogen-Activated Protein Kinase 3biologyERK1/2herceptinAntibodies MonoclonalCytochromes cImmunohistochemistrynude miceGene Expression Regulation NeoplasticOncologyTetracyclinesKi-67Ki-67Femalemedicine.drugmedicine.medical_specialtyBlotting WesternDown-RegulationMice NudeAntineoplastic AgentsProtein Serine-Threonine KinasesAntibodies Monoclonal Humanizedresistance3-Phosphoinositide-Dependent Protein Kinasesbreast cancerDownregulation and upregulationresponse to therapyInternal medicineHER2medicineAnimalsRNA Messengercytochrome c releaseProtein kinase Bneoplasmstumour developmentCell Proliferationhumanised monoclonal antibodyAktCancerMammary Neoplasms ExperimentalTrastuzumabmedicine.diseaseEndocrinologyKi-67 AntigenApoptosisDrug Resistance Neoplasmbiology.proteinCancer researchreceptor tyrosine kinaseTranslational TherapeuticsProto-Oncogene Proteins c-aktBritish Journal of Cancer
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