Search results for "Cell death"

showing 10 items of 824 documents

Surveillance of spontaneous breast cancer metastasis by TRAIL-expressing CD34⁺ cells in a xenograft model

2012

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), delivered as a membrane-bound molecule expressed on the surface of adenovirus-transduced CD34+ cells (CD34-TRAIL+), was analyzed for its apoptotic activity in vitro on 12 breast cancer cell lines representing estrogen receptor-positive, HER2+ and triple-negative (TN) subtypes and for its effect on tumor growth, vascularization, necrosis, and lung metastasis incidence in NOD/SCID mice xenografted with the TN breast cancer line MDA-MB-231. Mesenchymal TN cell lines, which are the richest in putative tumor stem cells among the different breast cancer cell subtypes, were the most susceptible to apoptosis induced by CD34-TRAIL+ cel…

PathologyCancer ResearchCD34Antigens CD34ApoptosisMice SCIDMetastasisMetastasisTNF-Related Apoptosis-Inducing LigandMicePreclinical StudyMice Inbred NODNeoplasm Metastasisskin and connective tissue diseasesHeterologousTumorbiologyCell DeathCancer stem cellsTumor BurdenOncologyNeoplastic Stem CellsTumor necrosis factor alphaFemalemedicine.medical_specialtyTRAIL BREAST CANCERTransplantation HeterologousBreast NeoplasmsSCIDCell LineTriple-negative breast cancerCancer stem cellCell Line TumormedicineAnimalsHumansAntigensTransplantationCD44Mesenchymal stem cellmedicine.diseaseApoptosisCell culturebiology.proteinCancer researchInbred NODCD34Settore MED/36 - Diagnostica Per Immagini E RadioterapiaAnimals; Antigens CD34; Apoptosis; Breast Neoplasms; Cell Death; Cell Line Tumor; Female; Humans; Mice; Mice Inbred NOD; Mice SCID; Neoplasm Metastasis; Neoplastic Stem Cells; TNF-Related Apoptosis-Inducing Ligand; Transplantation Heterologous; Tumor BurdenmTRAIL
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Neuronal and BBB damage induced by sera from patients with secondary progressive multiple sclerosis.

2009

An important component of the pathogenic process of multiple sclerosis (MS) is the blood-brain barrier (BBB) damage. We recently set an in vitro model of BBB, based on a three-cell-type co-culture system, in which rat neurons and astrocytes synergistically induce brain capillary endothelial cells to form a monolayer with permeability properties resembling those of the physiological BBB. Herein we report that the serum from patients with secondary progressive multiple sclerosis (SPMS) has a damaging effect on isolated neurons. This finding suggests that neuronal damaging in MS could be a primary event and not only secondary to myelin damage, as generally assumed. SPMS serum affects the perme…

Pathologymedicine.medical_specialtyProgrammed cell deathBlotting WesternBiologyImmunofluorescenceOccludinModels BiologicalMyelinWestern blotOccludinGeneticsmedicineElectric ImpedanceAnimalsmultiple sclerosis brain cell cultures in vitro models of blood-brain barrier neuronal cell death transendothelial electrical resistanceMicroscopy Phase-ContrastRats WistarCells CulturedNeuronsmedicine.diagnostic_testTight junctionCell DeathMultiple sclerosisMembrane ProteinsGeneral MedicineMultiple Sclerosis Chronic Progressivemedicine.diseaseImmunohistochemistryRatsBlotmedicine.anatomical_structurenervous systemBlood-Brain BarrierAstrocytescardiovascular systemInternational journal of molecular medicine
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Comparative study of T84 and T84SF human colon carcinoma cells: in vitro and in vivo ultrastructural and functional characterization of cell culture …

2005

To better understand the relationship between tumor heterogeneity, differentiation, and metastasis, suitable experimental models permitting in vitro and in vivo studies are necessary. A new variant cell line (T84SF) exhibiting an altered phenotype was recently selected from a colon cancer cell line (T84) by repetitive plating on TNF-alpha treated human endothelial cells and subsequent selection for adherent cells. The matched pair of cell lines provides a useful system to investigate the extravasation step of the metastatic cascade. Since analysis of morphological differences can be instructive to the understanding of metastatic potential of tumor cells, we compared the ultrastructural and …

Pathologymedicine.medical_specialtyProgrammed cell deathColon carcinoma ; Tumor cells;. Ultrastructure ; Metastasis .;Apoptosis . ;Bcl-XL;Bcl-XLbcl-X ProteinColon carcinomaApoptosis. UltrastructureBiologyAdenocarcinomaMetastasis .Pathology and Forensic MedicineMetastasischemistry.chemical_compoundMicroscopy Electron TransmissionIn vivoCell Line TumorTumor cellmedicineBiomarkers TumorHumansNeoplasm MetastasisMolecular BiologyCell NucleusCytoplasmic VesiclesTyrosine phosphorylationCell BiologyGeneral Medicinemedicine.diseaseApoptosis .In vitroPhenotypechemistryPleomorphism (cytology)ApoptosisCell cultureGelatinasesColonic NeoplasmsCancer researchDisease ProgressionSignal Transduction
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Neuroprotective effect of flupirtine in prion disease

2003

Apoptotic neuronal cell death is a hallmark of prion diseases. The apoptotic process in neuronal cells is thought to be caused by the scrapie prion protein, PrPSc, and can be experimentally induced by its peptide fragment, PrP106-126. This process is a target for potential drugs to combat prion disease or to ameliorate its symptoms. Flupirtine (Katadolon), a pyridine derivative that is in clinical use as a nonopioid analgesic, has a potent cytoprotective effect, at concentrations above 1 microg/mL, on neuronal cells treated with PrP(Sc) or PrP106-126. This drug acts as an N-methyl-D-aspartate (NMDA) antagonist, but does not bind to NMDA receptors. Flupirtine normalizes the level of intracel…

Pathologymedicine.medical_specialtyProgrammed cell deathanimal diseasesAnalgesicAminopyridinesScrapiePharmacologyNeuroprotectionPrion DiseasesmedicineAnimalsHumansPharmacology (medical)Pharmacologybusiness.industryAntagonistGeneral MedicineGlutathioneGenes bcl-2nervous system diseasesNeuroprotective Agentsnervous systemApoptosisNMDA receptorCalciumFlupirtinebusinessmedicine.drugDrugs of Today
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Role of mitochondria in parvovirus pathology.

2014

Proper functioning of the mitochondria is crucial for the survival of the cell. Viruses are able to interfere with mitochondrial functions as they infect the host cell. Parvoviruses are known to induce apoptosis in infected cells, but the role of the mitochondria in parvovirus induced cytopathy is only partially known. Here we demonstrate with confocal and electron microscopy that canine parvovirus (CPV) associated with the mitochondrial outer membrane from the onset of infection. During viral entry a transient depolarization of the mitochondrial transmembrane potential and increase in ROS level was detected. Subsequently, mitochondrial homeostasis was normalized shortly, as detected by rep…

PathologyvirusesCelllcsh:MedicineMitochondrionSignal transductionERK signaling cascadeMolecular cell biologyInner mitochondrial membraneExtracellular Signal-Regulated MAP Kinaseslcsh:SciencepatologiaCellular Stress ResponsesMembrane Potential MitochondrialMultidisciplinarybiologyCell DeathCanine parvovirusapoptosisSignaling cascadesCellular StructuresCell biologyMitochondriaHost-Pathogen Interactionmedicine.anatomical_structureMitochondrial MembranesResearch Articlemedicine.medical_specialtyViral EntryParvovirus CanineMAP Kinase Signaling SystemmitokondriotMicrobiologyCell LineParvoviridae InfectionsDogsViral entryVirologymedicineAnimalsBiologysoluviestintäParvovirusta1183parvoviruslcsh:Rta1182biology.organism_classificationMolecular biologyEnzyme ActivationViral replicationSubcellular OrganellesApoptosisCatsCalciumlcsh:QReactive Oxygen SpeciesViral Transmission and InfectionPLoS ONE
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Synthesis and photocytotoxic activity of [1,2,3]triazolo[4,5-h][1,6]naphthyridines and [1,3]oxazolo[5,4-h][1,6]naphthyridines

2018

Abstract [1,2,3]Triazolo[4,5-h][1,6]naphthyridines and [1,3]oxazolo[5,4-h][1,6]naphthyridines were synthesized with the aim to investigate their photocytotoxic activity. Upon irradiation, oxazolo-naphtapyridines induced light-dependent cell death at nanomolar/low micromolar concentrations (EC50 0.01–6.59 μM). The most photocytotoxic derivative showed very high selectivity and photocytotoxicity indexes (SI = 72–86, PTI>5000), along with a triplet excited state with exceptionally long lifetime (18.0 μs) and high molar absorptivity (29781 ± 180 M−1cm−1 at λmax 315 nm). The light-induced production of ROS promptly induced an unquenchable apoptotic process selectively in tumor cells, with mitoch…

Pharmaceutical ScienceApoptosisMitochondrionPhotochemiotherapy; Photosensitizing agents; Reactive oxygen species; [123]Triazolo[45-h][16]naphthyridines; [13]oxazolo[54-h][16]naphthyridines; Pharmacology; Drug Discovery; Pharmaceutical Science; Organic Chemistry01 natural sciencesMedicinal chemistry[13]oxazolo[54-h][16]naphthyridinechemistry.chemical_compoundDrug Discovery6]naphthyridineschemistry.chemical_classification0303 health sciencesTumorPhotosensitizing AgentsCell DeathSinglet OxygenSinglet oxygenPhotochemiotherapy; Photosensitizing agents; Reactive oxygen species; [1; 2; 3]Triazolo[4; 5-h][1; 6]naphthyridines; [1; 3]oxazolo[5; 4-h][1; 6]naphthyridines; Apoptosis; Cell Death; Cell Line; Tumor; Humans; Lysosomes; Mitochondria; Naphthyridines; Photochemotherapy; Photosensitizing Agents; Reactive Oxygen Species; Singlet OxygenGeneral MedicineLysosomeMitochondriaExcited stateReactive oxygen specie5-h][1HumanProgrammed cell death2NaphthyridinePhotochemiotherapy3]Triazolo[4Cell Line03 medical and health sciences4-h][1Cell Line TumorHumansNaphthyridines030304 developmental biologyPharmacologyReactive oxygen speciesPhotosensitizing agent010405 organic chemistryOrganic ChemistryApoptosi0104 chemical sciences3]oxazolo[5chemistryPhotochemotherapyCell cultureApoptosis[123]Triazolo[45-h][16]naphthyridine[1LysosomesReactive Oxygen SpeciesDerivative (chemistry)
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N-acetylglycoside of oleanolic acid (aridanin) displays promising cytotoxicity towards human and animal cancer cells, inducing apoptotic, ferroptotic…

2020

Abstract Background The discovery of novel phytochemicals represents a reasonable approach to fight malignancies, especially those which are resistant to standard chemotherapy. Purpose We evaluated the cytotoxic potential of a naturally occurring N-acetylglycoside of oleanolic acid, aridanin, on 18 cancer cell lines, including sensitive and drug-resistant phenotypes mediated by P-glycoprotein, BCRP, p53 knockout, deletion-mutated EGFR, or BRAF mutations. Furthermore, metastasizing B16/F10 cells, HepG2 hepatocarcinoma and normal AML12 hepatocytes were investigated. The mechanisms of aridanin-induced cell death was further investigated. Methods The resazurin reduction assay (RRA) was applied …

Pharmacology0303 health sciencesProgrammed cell deathbiologyChemistryNecroptosisPharmaceutical ScienceCell cycle03 medical and health sciences0302 clinical medicineComplementary and alternative medicineApoptosis030220 oncology & carcinogenesisDrug DiscoveryCancer cellbiology.proteinCancer researchMolecular MedicineCytotoxic T cellCytotoxicityCaspase030304 developmental biologyPhytomedicine
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Cucurbitacins as inducers of cell death and a rich source of potential anticancer compounds.

2011

Triterpenes have been reported to induce cell death. One relevant group of this family of compounds is cucurbitacins, which have been studied as inducers of apoptosis in various cancer cell lines. The most significant mechanisms with regard to the apoptotic effects of cucurbitacins are their ability to modify transcriptional activities via nuclear factors or genes and their capability to activate or inhibit pro- or anti-apoptotic proteins. Still, while the majority of studies on these compounds have dealt with their apoptotic effects on cancer cell lines, several research groups have also explored their anti-inflammatory activities. In general, cucurbitacins are considered to be selective i…

PharmacologyMAPK/ERK pathwayProgrammed cell deathCell CycleApoptosisCucurbitacinsCell cycleBiologyAntineoplastic Agents PhytogenicstatCell biologyCucurbitacinsApoptosisDrug Discoverybiology.proteinAnimalsHumansCyclin D3STAT3Signal TransductionCurrent pharmaceutical design
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Enhanced oxidative stress and increased mitochondrial mass during Efavirenz-induced apoptosis in human hepatic cells

2010

BACKGROUND AND PURPOSE Efavirenz (EFV) is widely used in the treatment of HIV-1 infection. Though highly efficient, there is growing concern about EFV-related side effects, the molecular basis of which remains elusive. EXPERIMENTAL APPROACH In vitro studies were performed to address the effect of clinically relevant concentrations of EFV (10, 25 and 50 µM) on human hepatic cells. KEY RESULTS Cellular proliferation and viability were reduced in a concentration-dependent manner. Analyses of the cell cycle and several cell death parameters (chromatin condensation, phosphatidylserine exteriorization, mitochondrial proapoptotic protein translocation and caspase activation) revealed that EFV trig…

PharmacologyMitochondrial DNAProgrammed cell deathMitochondrionBiologymedicine.diseasemedicine.disease_causeCell biologyMitochondrial toxicitychemistry.chemical_compoundchemistryBiochemistryApoptosismedicineCardiolipinOxidative stressMitochondrial DNA replicationBritish Journal of Pharmacology
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Flupirtine increases the levels of glutathione and Bcl-2 in hNT (human ) neurons: mode of action of the drug-mediated anti-apoptotic effect

1996

Flupirtine is a triaminopyridine analogue which has been successfully applied in clinics as a non-opiate analgesic drug. Previously we described that flupirtine acts like an N-methyl-D-aspartate (NMDA) receptor antagonist in neuronal cells both in vitro and in vivo. Here we show that flupirtine displays its anti-apoptotic effect also in hNT (human Ntera/D1) neurons. hNT neurons were induced to apoptosis applying glutamate (Glu; at concentrations > or = 1 mM) or NMDA (> or = 1 mM). During Glu/NMDA-mediated apoptosis the levels of the intracellular anti-apoptotic agents Bc1-2 and glutathione dropped by more than 50%. Flupirtine completely abolished this reduction of Bc1-2 and glutathione leve…

PharmacologyProgrammed cell deathChemistrymedicine.drug_classGlutamate receptorGlutathionePharmacologyReceptor antagonistchemistry.chemical_compoundmedicine.anatomical_structurenervous systemBiochemistryMechanism of actionmedicineNMDA receptorNeuronFlupirtinemedicine.symptommedicine.drugEuropean Journal of Pharmacology
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