Search results for "programmed cell death"

showing 10 items of 609 documents

DNA Damage Response and the Balance Between Cell Survival and Cell Death

2009

DNA damage induces the activation of a cascade of kinases that trigger the DNA damage response (DDR). Downstream are targets that either help cells to survive or undergo cell death. DNA damage-induced cell death is executed by apoptosis, necrosis, mitotic catastrophe, and autophagy. Of these different forms of cell inactivation, apoptosis is often the main route of cell death following DNA damage. Cells undergo apoptosis upon genotoxic stress via the death receptor and/or the intrinsic mitochondrial damage pathway, with p53 and AP-1 involved decisively. Not every type of DNA damage induces apoptosis. Many DNA lesions are tolerated by the cell, some are mutagenic without being toxic and some…

Programmed cell deathmedicine.anatomical_structureApoptosisDNA damageDNA repairCellmedicineGenotoxic StressCell cycleBiologyMitotic catastropheCell biology
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Tumor Cytotoxicity by Endothelial Cells

2003

High GSH content associates with high metastatic activity in B16-F10 melanoma cells cultured to low density (LD B16M). GSH homeostasis was investigated in LD B16M cells that survive after adhesion to the hepatic sinusoidal endothelium (HSE). Invasive B16M (iB16M) cells were isolated using anti-Met-72 monoclonal antibodies and flow cytometry-coupled cell sorting. HSE-derived NO and H(2)O(2) caused GSH depletion and a decrease in gamma-glutamylcysteine synthetase activity in iB16M cells. Overexpression of gamma-glutamylcysteine synthetase heavy and light subunits led to a rapid recovery of cytosolic GSH, whereas mitochondrial GSH (mtGSH) further decreased during the first 18 h of culture. NO …

Programmed cell deathmedicine.diagnostic_testLiver cytologyCell BiologyGlutathioneBiologymedicine.disease_causeBiochemistryIn vitroCell biologyFlow cytometrychemistry.chemical_compoundCytosolchemistrymedicineMolecular BiologyHomeostasisOxidative stressJournal of Biological Chemistry
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Programmed cell death (PCD) associated with the stilbene motif of arotinoids: discovery of novel apoptosis inducer agents possessing activity on mult…

2000

Considering that the stereochemistry of the C9-C10 alkenyl portion of natural 9-cis-RA, as the one of the olefinic moiety of the previously described isoxazole retinoid 4, seems of particular importance for their apoptotic activity, we prepared a novel class of TTNPB analogues bearing both the cis or trans configuration of the alkenyl portion. The compounds were evaluated in vitro for their cytotoxic and apoptotic activities. We discovered that the cis-TTNPB 9c possesses apoptotic activity comparable with that of the retinoid 4. Moreover, the amino arotinoid 16c showed potent apoptotic activity in HL60 promyelocytic leukemia cells. Interestingly, 16c proved to be a particularly potent apopt…

Programmed cell deathmedicine.drug_classHL60Clinical BiochemistryPharmaceutical ScienceAntineoplastic AgentsApoptosisHL-60 CellsBiochemistryRetinoidschemistry.chemical_compoundStilbenesDrug DiscoverymedicineHumansCytotoxic T cellRetinoidCytotoxicityMolecular BiologyChemistryOrganic ChemistryDrug Resistance MultipleMultiple drug resistanceBiochemistryApoptosisCell cultureMolecular MedicineK562 CellsBioorganic & Medicinal Chemistry Letters
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Berberine inhibits cell growth and mediates caspase-independent cell death in human pancreatic cancer cells.

2010

Pancreatic cancer is one of the most aggressive human malignancies with an increasing incidence worldwide. In addition to the poor survival rates, combinations using gemcitabine as a backbone have failed to show any benefit beyond monotherapy. These facts underscore an urgent need for novel therapeutic options and motivated us to study the effect of berberine on pancreatic cancer cells. Here, we undertook an mRNA-based gene expression profiling study in order to get deeper insight into the molecular targets mediating the growth inhibitory effects of berberine on pancreatic cancer cells compared to normal ones. Twenty-four hours after treatment, berberine showed preferential selectivity towa…

Programmed cell deathmedicine.medical_specialtyBerberineDNA damagePharmaceutical ScienceApoptosisAnalytical Chemistrychemistry.chemical_compoundBerberinePancreatic cancerInternal medicineCell Line TumorDrug DiscoverymedicineHumansRNA MessengerCell ProliferationOligonucleotide Array Sequence AnalysisPharmacologybiologyCell growthTopoisomeraseGene Expression ProfilingOrganic ChemistryCancermedicine.diseaseAntineoplastic Agents PhytogenicCaspase InhibitorsImmunohistochemistryEnzyme ActivationPancreatic NeoplasmsEndocrinologyComplementary and alternative medicinechemistryApoptosisCaspasesbiology.proteinCancer researchMolecular MedicineSignal TransductionPlanta medica
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Peroxisome proliferator-activated receptor δ (PPARδ) activation protects H9c2 cardiomyoblasts from oxidative stress-induced apoptosis

2005

Activation of peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARgamma plays beneficial roles in cardiovascular disorders such as atherosclerosis and heart reperfusion. Although PPARalpha and gamma have been documented to reduce oxidative stress in the vasculature and the heart, the role of PPARdelta remains poorly studied.We focused on PPARdelta function in the regulation of oxidative stress-induced apoptosis in the rat cardiomyoblast cell line H9c2. Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), we showed that PPARdelta is the predominantly expressed isotype whereas PPARalpha was weakly detected. By performing cell viability assays, we …

Programmed cell deathmedicine.medical_specialtyPhysiologyBlotting WesternPeroxisome proliferator-activated receptorApoptosisCaspase 3DNA FragmentationBiologyTransfectionmedicine.disease_causeCell LineGW501516Physiology (medical)Internal medicineIn Situ Nick-End LabelingmedicineAnimalsPPAR deltaViability assayReceptorchemistry.chemical_classificationCaspase 3Reverse Transcriptase Polymerase Chain ReactionHydrogen PeroxideCatalasemedicine.diseaseRatsUp-RegulationCell biologyOxidative StressThiazolesEndocrinologychemistryApoptosisCaspasesCardiology and Cardiovascular MedicineMyoblasts CardiacOxidative stressCardiovascular Research
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Transmembrane BAX Inhibitor-1 Motif Containing Protein 5 (TMBIM5) Sustains Mitochondrial Structure, Shape, and Function by Impacting the Mitochondria…

2020

The Transmembrane Bax Inhibitor-1 motif (TMBIM)-containing protein family is evolutionarily conserved and has been implicated in cell death susceptibility. The only member with a mitochondrial localization is TMBIM5 (also known as GHITM or MICS1), which affects cristae organization and associates with the Parkinson&rsquo

Programmed cell deathmitochondrial metabolismProtein familyApoptosisMitochondrioncell survivalArticleGHITMMitochondrial ProteinsTMBIMHumansInner mitochondrial membranelcsh:QH301-705.5bcl-2-Associated X ProteinBAX inhibitor 1ChemistryMembrane ProteinsGeneral MedicineTransmembrane proteinCell biologyDNA-Binding Proteinsmitochondriacell deathMitochondrial biogenesislcsh:Biology (General)Mitochondrial Membranes
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Fatty acids liberated from low-density lipoprotein trigger endothelial apoptosis via mitogen-activated protein kinases.

2005

Enzymatic modification of low-density lipoprotein (LDL) as it probably occurs in the arterial intima drastically increases its cytotoxicity, which could be relevant for the progression of atherosclerotic lesions. LDL was treated with a protease and cholesterylesterase to generate a derivative similar to lesional LDL, with a high content of free cholesterol and fatty acids. Exposure of endothelial cells to the enzymatically modified lipoprotein (E-LDL), but not to native or oxidized LDL, resulted in programmed cell death. Apoptosis was triggered by apoptosis signal-regulating kinase 1 dependent phosphorylation of p38. Depletion and reconstitution experiments identified free fatty acids (FFA)…

Programmed cell deathp38 mitogen-activated protein kinasesBlotting WesternApoptosisDNA FragmentationBiologyFatty Acids NonesterifiedMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundHumansPhosphorylationMolecular BiologyCells CulturedCaspase 7Cell growthKinaseCaspase 3Cell BiologyCell biologyLipoproteins LDLchemistryBiochemistryApoptosisLow-density lipoproteinCaspasesPhosphorylationlipids (amino acids peptides and proteins)Endothelium VascularLipoproteinOleic AcidCell death and differentiation
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Silymarin and Cancer: A Dual Strategy in Both in Chemoprevention and Chemosensitivity

2020

Silymarin extracted from milk thistle consisting of flavonolignan silybin has shown chemopreventive and chemosensitizing activity against various cancers. The present review summarizes the current knowledge on the potential targets of silymarin against various cancers. Silymarin may play on the system of xenobiotics, metabolizing enzymes (phase I and phase II) to protect normal cells against various toxic molecules or to protect against deleterious effects of chemotherapeutic agents on normal cells. Furthermore, silymarin and its main bioactive compounds inhibit organic anion transporters (OAT) and ATP-binding cassettes (ABC) transporters, thus contributing to counteracting potential chemor…

Programmed cell deathsilymarinCellChemosensitizerPharmaceutical SciencechemopreventiveATP-binding cassette transporterApoptosisReviewProtective AgentsChemopreventionsilybinAnalytical Chemistrylcsh:QD241-44103 medical and health sciences0302 clinical medicinelcsh:Organic chemistryDrug DiscoverymedicineHumansPhysical and Theoretical ChemistryReceptor030304 developmental biology0303 health sciencesChemistryOrganic ChemistryCancerCell Cycle CheckpointsCell cyclemedicine.diseasemedicine.anatomical_structureChemistry (miscellaneous)intrinsic and extrinsic pathwayDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellchemosensitizerCancer researchMolecular Medicinemetabolizing enzymesATP-Binding Cassette Transporterscell cycleABC transporterSignal TransductionMolecules
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TRAIL-R4 promotes tumor growth and resistance to apoptosis in cervical carcinoma HeLa cells through AKT.

2011

International audience; BACKGROUND: TRAIL/Apo2L is a pro-apoptotic ligand of the TNF family that engages the apoptotic machinery through two pro-apoptotic receptors, TRAIL-R1 and TRAIL-R2. This cell death program is tightly controlled by two antagonistic receptors, TRAIL-R3 and TRAIL-R4, both devoid of a functional death domain, an intracellular region of the receptor, required for the recruitment and the activation of initiator caspases. Upon TRAIL-binding, TRAIL-R4 forms a heteromeric complex with the agonistic receptor TRAIL-R2 leading to reduced caspase-8 activation and apoptosis. METHODOLOGY/PRINCIPAL FINDINGS: We provide evidence that TRAIL-R4 can also exhibit, in a ligand independent…

Proliferation indexlcsh:MedicineTNF-Related Apoptosis-Inducing LigandHeLaMicePhosphatidylinositol 3-Kinases0302 clinical medicineMolecular Cell BiologyBasic Cancer ResearchMembrane Receptor SignalingEnzyme Inhibitorslcsh:SciencePhosphoinositide-3 Kinase Inhibitors0303 health sciencesMultidisciplinaryCell Deathbiologyapoptosis3. Good healthCell biologyOncology030220 oncology & carcinogenesisMedicineFemaleSignal transductionResearch ArticleSignal TransductionProgrammed cell deathMorpholinesproliferationBlotting WesternMice Nude03 medical and health sciencesTRAIL-R4[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyBiology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biologyCell growthAktCell Membranelcsh:RPTEN PhosphohydrolaseNeoplasms Experimentalbiology.organism_classificationTumor Necrosis Factor Decoy ReceptorsChromonesApoptosislcsh:QProto-Oncogene Proteins c-aktHeLa Cells
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Apoptosis in liver disease

2001

A variety of biological functions are regulated through extracellular signals. Amongst the best studied examples is growth control, which is achieved by the regulatory function of growth factors. In recent years it has become apparent that cell death (apoptosis) is controlled in a similar fashion. Apoptosis, firstly a morphologically defined process, is a highly controlled type of cell death that plays a critical role in embryonic development, deletion of autoreactive T-cells and adult tissue homoeostasis. There is increasing evidence that derangement of the apoptotic program is the underlying cause of a series of diseases including liver diseases. The deadly program can be initiated by lig…

ProteasesProgrammed cell deathApoptosisLigandsReceptors Tumor Necrosis FactorFas ligandTransforming Growth Factor beta1Antigens CDTransforming Growth Factor betaExtracellularAnimalsHumansfas ReceptorCaspaseHepatologybiologyLiver DiseasesGastroenterologyFas receptorCell biologyBiochemistryReceptors Tumor Necrosis Factor Type IApoptosisCaspasesbiology.proteinIntracellularEuropean Journal of Gastroenterology & Hepatology
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