Search results for "KINASE"

showing 10 items of 2635 documents

Aspidin PB, a phloroglucinol derivative, induces apoptosis in human hepatocarcinoma HepG2 cells by modulating PI3K/Akt/GSK3β pathway.

2012

Aspidin PB, a phloroglucinol derivative isolated from Dryopteris fragrans (L.) Schott, has been previously reported to exert high biological activities. In the present study, we analyzed the apoptotic mechanisms of aspidin PB on human hepatoma cell line, HepG2. Initially, aspidin PB was shown to inhibit the growth of HepG2 cells in a time and dose-dependent manner. After treatment with aspidin PB for 72 h, 48 h and 24 h using MTT assay, the IC(50) values were 10.59 μM, 20.86 μM and 46.59 μM, respectively. Aspidin PB was capable to induce apoptosis, as measured by mitochondrial membrane potential (ΔΨm), acridine orange (AO) staining and propidium iodide (PI)/annexin V-FITC double staining. T…

Carcinoma HepatocellularApoptosisBiologyPhloroglucinolToxicologyWortmanninchemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesAnnexinHumansMTT assayPropidium iodideProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationPhosphoinositide-3 Kinase InhibitorsMembrane Potential MitochondrialGlycogen Synthase Kinase 3 betaMicroscopy ConfocalAcridine orangeLiver NeoplasmsGeneral MedicineHep G2 CellsFlow CytometryMolecular biologyAndrostadieneschemistryApoptosisWortmanninProto-Oncogene Proteins c-aktSignal TransductionChemico-biological interactions
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The Synthetic Cannabinoid WIN 55,212-2 Sensitizes Hepatocellular Carcinoma Cells to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-I…

2010

In this article, we demonstrate that the synthetic cannabinoid R-(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)-(1-naphthalenyl) methanone mesylate (WIN 55,212-2) sensitizes human hepatocellular carcinoma (HCC) cells to apoptosis mediated by tumor necrosis-related apoptosis inducing ligand (TRAIL). The apoptotic mechanism induced by treatment with WIN/TRAIL combination involved the loss of the mitochondrial transmembrane potential and led to the activation of caspases. In HCC cells, WIN treatment induced the up-regulation of TRAIL death receptor DR5, an effect that seemed to be related to the increase in the level of p8 and CHOP, two factors implicat…

Carcinoma HepatocellularDNA ComplementaryMorpholinesApoptosisNaphthalenesCHOPMembrane PotentialsTNF-Related Apoptosis-Inducing LigandCell Line TumorSurvivinmedicineHumansWIN 55212-2Protein kinase BTranscription factorCaspaseDNA PrimersPharmacologybiologyCannabinoidsReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsGene AmplificationDNA NeoplasmFlow CytometryBenzoxazinesReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMitochondrial MembranesImmunologybiology.proteinCancer researchMolecular MedicineTumor necrosis factor alphaTranscription Factor CHOPmedicine.drugMolecular Pharmacology
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Analysis of Possible Mechanisms Accounting for Raf-1 Kinase Inhibitor Protein Downregulation in Hepatocellular Carcinoma

2012

Abstract Raf-1 kinase inhibitor protein (RKIP) is a tumor and metastasis suppressor that promotes drug-induced apoptosis in cancer cells. It is frequently downregulated, both at the mRNA and protein level, in hepatocellular carcinoma (HCC), but the mechanisms leading to this reduction are obscure. We sequenced the whole RKIP gene in three human HCC cell lines (HA22T/VGH, HepG2, and Hep3B), and in five clinical HCC samples, but could not find any gene variant that might account for their low RKIP levels. We also examined whether gene methylation may be responsible for the altered RKIP expression. No methylation of the RKIP gene was found in the tumor samples, while among the cell lines only …

Carcinoma HepatocellularLeupeptinsAntineoplastic AgentsPhosphatidylethanolamine Binding ProteinRKIP (Raf-1 kinase inhibitor protein) hepatocellular carcinomaBiologyBiochemistryDownregulation and upregulationRNA interferenceCell Line TumorGeneticsHumansMetastasis suppressorPromoter Regions GeneticMolecular BiologyRegulation of gene expressionKinaseLiver NeoplasmsHep G2 CellsMethylationDNA Methylationdigestive system diseasesGene Expression Regulation NeoplasticMicroRNAsMutationCancer cellDNA methylationAzacitidineSettore BIO/14 - FarmacologiaCancer researchMolecular MedicineRNA InterferenceBiotechnologyOMICS: A Journal of Integrative Biology
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Intracoronary application of C1 esterase inhibitor improves cardiac function and reduces myocardial necrosis in an experimental model of ischemia and…

1997

Background Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events, including complement activation, leukocyte adhesion, and infiltration and release of diverse mediators, probably play important roles. The present study addresses the possibility of reducing reperfusion damage by the application of C1 esterase inhibitor (C1-INH). Methods and Results Cardioprotection by C1-INH 20 IU/kg IC was examined in a pig model with 60 minutes of coronary occlusion, followed by 120 minutes of reperfusion. C1-INH was administered during the first 5 minutes of coronary reperfusion…

Cardiac function curveMalemedicine.medical_specialtyAnaphylatoxinsNecrosisSwinePartial PressureIschemiaMyocardial IschemiaMyocardial ReperfusionComplement C1 Inactivator ProteinsCreatineInjectionschemistry.chemical_compoundNecrosisTroponin TPhysiology (medical)Internal medicinemedicineAnimalsMyocardial infarctionLactic AcidCreatine KinaseCardioprotectionTroponin Tbusiness.industryMyocardiumHemodynamicsHeartmedicine.diseaseCoronary VesselsTroponinOxygenchemistryCoronary occlusionAnesthesiaCardiologyFemalemedicine.symptomCardiology and Cardiovascular MedicinebusinessCirculation
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Supraventricular tachycardias, conduction disease, and cardiomyopathy in 3 families with the same rare variant in TNNI3K (p.Glu768Lys)

2018

IF 4.743 (2017); International audience; BackgroundRare genetic variants in TNNI3K encoding troponin-I interacting kinase have been linked to a distinct syndrome consisting primarily of supraventricular tachycardias and variably expressed conduction disturbance and dilated cardiomyopathy in 2 families.ObjectiveThe purpose of this study was to identify new genetic variants associated with inherited supraventricular tachycardias, cardiac conduction disease, and cardiomyopathy.MethodsWe conducted next generation sequencing in 3 independent multigenerational families with atrial/junctional tachycardia with or without conduction disturbance, dilated cardiomyopathy, and sudden death. We also asse…

Cardiomyopathy DilatedMaleKinaseAdolescentConduction diseaseBlotting WesternDNA Mutational AnalysisCardiomyopathyDilated cardiomyopathyMagnetic Resonance Imaging Cine030204 cardiovascular system & hematologyProtein Serine-Threonine KinasesSudden death03 medical and health sciencesYoung Adult0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemHeart Conduction SystemPhysiology (medical)Cardiac conductionmedicineTachycardia SupraventricularGeneticsHumans030212 general & internal medicineGenetic TestingKinase activityCells CulturedGeneticsbusiness.industryRare variantTNNI3KDilated cardiomyopathyDNAmedicine.diseasePedigreeProtein autophosphorylationSupraventricular tachycardiaJunctional tachycardiaMutationFemaleSupraventricular tachycardiaCardiology and Cardiovascular Medicinebusiness
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Deleting Full Length Titin Versus the Titin M-Band Region Leads to Differential Mechanosignaling and Cardiac Phenotypes

2019

Background: Titin is a giant elastic protein that spans the half-sarcomere from Z-disk to M-band. It acts as a molecular spring and mechanosensor and has been linked to striated muscle disease. The pathways that govern titin-dependent cardiac growth and contribute to disease are diverse and difficult to dissect. Methods: To study titin deficiency versus dysfunction, the authors generated and compared striated muscle specific knockouts (KOs) with progressive postnatal loss of the complete titin protein by removing exon 2 (E2-KO) or an M-band truncation that eliminates proper sarcomeric integration, but retains all other functional domains (M-band exon 1/2 [M1/2]-KO). The authors evaluated c…

Cardiomyopathy DilatedMaleSarcomeresanimal structuresVentricular Dysfunction Rightmacromolecular substances030204 cardiovascular system & hematologyMechanotransduction CellularVentricular Function LeftArticleMuscle hypertrophyVentricular Dysfunction Left03 medical and health sciences0302 clinical medicinePhysiology (medical)AnimalsMedicineMyocytes CardiacMuscle Skeletal030304 developmental biologyMice Knockout0303 health sciencesbiologybusiness.industryMolecular springmusculoskeletal systemPhenotypeCell biologyMuscular AtrophyPhenotypeMuscle diseasecardiovascular systemVentricular Function Rightbiology.proteinTitinCardiology and Cardiovascular MedicinebusinessProtein KinasesGene DeletionDifferential (mathematics)Circulation
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Nitroglycerin-induced cardioprotection is endothelial nitric oxide synthase- dependent

2015

Purpose We sought to evaluate the contribution of the endogenous NO pathway to the cardioprotective action of nitroglycerin (NTG). Methods and Results Anesthetized rabbits were subjected to 30-min myocardial ischemia (isc) and 3-h reperfusion (rep) and randomized into: Control group (no further intervention); PostC group (application of 8 cycles 30-sec isc/rep) and NTG treated group (2 μg/kg-1/min-1 IV bolus) for 65 min starting 10 min prior to rep. In additional groups, pharmacological inhibitors of NOS, nNOS, iNOS, PI3K, adenosine receptors and PKG were administrated with or without NTG. The infarcted (I) to risk (R) ratio was estimated. In a second experimental series tissue samples were…

Cardioprotectiongenetic structuresbiologybusiness.industryNitrotyrosineEndogenyPharmacologybiology.organism_classificationBiochemistryAdenosine receptoreye diseaseschemistry.chemical_compoundBolus (medicine)chemistryEnosPhysiology (medical)AnesthesiaMedicinebusinessProtein kinase BPI3K/AKT/mTOR pathwayFree Radical Biology and Medicine
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Cardioprotection by gene therapy

2015

Ischemic heart disease remains the leading cause of death worldwide. Ischemic pre-, post-, and remote conditionings trigger endogenous cardioprotection that renders the heart resistant to ischemic-reperfusion injury (IRI). Mimicking endogenous cardioprotection by modulating genes involved in cardioprotective signal transduction provides an opportunity to reproduce endogenous cardioprotection with better possibilities of translation into the clinical setting. Genes and signaling pathways by which conditioning maneuvers exert their effects on the heart are partially understood. This is due to the targeted approach that allowed identifying one or a few genes associated with IRI and cardioprote…

Cardioprotectionmedicine.medical_specialtybiologybusiness.industryGene targetingSphingosine kinase 1Heat shock proteinInternal medicineGene expressionmedicinebiology.proteinCardiologyHepatocyte growth factorSignal transductionCardiology and Cardiovascular MedicinebusinessTranscription factormedicine.drugInternational Journal of Cardiology
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Cardioprotective effects of phytopigments via multiple signaling pathways.

2021

Abstract Background Cardiovascular diseases (CVDs) are among the deadliest non-communicable diseases, and millions of dollars are spent every year to combat CVDs. Unfortunately, the multifactorial etiology of CVDs complicates the development of efficient therapeutics. Interestingly, phytopigments show significant pleiotropic cardioprotective effects both in vitro and in vivo. Purpose This review gives an overview of the cardioprotective effects of phytopigments based on in vitro and in vivo studies as well as clinical trials. Methods A literature-based survey was performed to collect the available data on cardioprotective activities of phytopigments via electronic search engines such as Pub…

Cardiotonic AgentsPharmaceutical ScienceAnthraquinonesXanthophyllsBioinformaticsstatAntioxidantsAnthocyaninsDrug DiscoveryMedicineAnimalsHumansClinical efficacyProtein kinase BPharmacologyFlavonoidsbusiness.industryNF-kappa BAMPKCarotenoidsClinical trialComplementary and alternative medicineCardiotoxicitiesCardiac hypertrophyMolecular MedicineSignal transductionbusinessSignal TransductionPhytomedicine : international journal of phytotherapy and phytopharmacology
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Synergistic Effect of Carfilzomib and Metformin in Vascular Plasticity; The Emerging Role of Autophagy

2019

Introduction: Carfilzomib (Cfz) correlates with a risk of reversible cardiotoxicity in 5-10% of multiple myeloma (MM) patients. We have recently shown that metformin (Met) has a prophylactic role against the Cfz-induced cardiotoxicity in vivo, through activation of AMPKα signaling (Blood 2019;133:710-23). However, the impact of Cfz on vascular function is obscure. Therefore, we sought to investigate: i) the acute, ii) the sub-chronic effect of Cfz on the vascular reactivity, iii) the effect of metformin co-administration on the vascular phenotype and iv) the impact of Cfz and Met co-administration on aged Human Aortic Smooth Muscle Cells (HAoSMCs). Methods: Forty male C57Bl/6 mice were assi…

CardiotoxicityMulticatalytic endopeptidase complexbusiness.industryMTOR Serine-Threonine KinasesImmunologyAutophagyCell BiologyHematologyBiochemistryCarfilzomibAngiotensin IIMetforminchemistry.chemical_compoundchemistryAnimals laboratoryCancer researchmedicinebusinessmedicine.drugBlood
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