Search results for "In Situ Nick-End Labeling"

showing 10 items of 49 documents

Lack of the Cell-Cycle Inhibitor p27Kip1 Results in Selective Increase of Transit-Amplifying Cells for Adult Neurogenesis

2002

The subventricular zone (SVZ) is the largest germinal layer in the adult mammalian brain and comprises stem cells, transit-amplifying progenitors, and committed neuroblasts. Although the SVZ contains the highest concentration of dividing cells in the adult brain, the intracellular mechanisms controlling their proliferation have not been elucidated. We show here that loss of the cyclin-dependent kinase inhibitor p27Kip1 has very specific effects on a population of CNS progenitors responsible for adult neurogenesis. Using bromodeoxyuridine and [3H]thymidine incorporation to label cells in S phase and cell-specific markers and electron microscopy to identify distinct cell types, we compared th…

MaleCell typePopulationSubventricular zoneApoptosisCell CountCell Cycle ProteinsMice TransgenicBiologyMicechemistry.chemical_compoundNeuroblastLateral VentriclesSpheroids CellularIn Situ Nick-End LabelingmedicineAnimalsARTICLEProgenitor celleducationCells CulturedNeuronseducation.field_of_studyStem CellsTumor Suppressor ProteinsGeneral NeuroscienceCell CycleNeurogenesisCell DifferentiationImmunohistochemistryCell biologyMice Inbred C57BLmedicine.anatomical_structureBromodeoxyuridinenervous systemchemistryStem cellCell DivisionCyclin-Dependent Kinase Inhibitor p27BromodeoxyuridineThymidineThe Journal of Neuroscience
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Modification of the rat aortic wall during ageing; possible relation with decrease of peptidergic innervation.

2002

Structural changes of the male rat aorta were followed from birth to old age in male and female rats. In males, the vessel media width and area progressively increase concomitantly with a decrease of nuclei density during ageing, suggesting an hypertrophy of the smooth muscle cells. These correlations were however not evidenced in females. TUNEL-positive cells were found in media of 4 and 6 months in both sexes, mainly on the luminal side and in the adventitia. When biochemical markers were investigated with immunohistochemistry, media was uniformly stained by the anti-vimentin and anti-alpha-smooth actin at all stages investigated. On the contrary, the surface of media stained with anti-de…

MaleEmbryologymedicine.medical_specialtyAgingEndotheliumVasoactive intestinal peptideDNA FragmentationCalcitonin gene-related peptideBiologyMuscle Smooth VascularMuscle hypertrophyDesminExtracellular matrixInternal medicineAdventitiamedicineIn Situ Nick-End LabelingAnimalsVimentinRats WistarAortaSex CharacteristicsNeuropeptidesCell BiologyHypertrophyNeuropeptide Y receptorImmunohistochemistryActinsRatsmedicine.anatomical_structureEndocrinologyAnimals NewbornAgeingFemaleEndothelium VascularAnatomyBiomarkersDevelopmental BiologyAnatomy and embryology
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Activation of the Proapoptotic Unfolded Protein Response in Plaques of the Human Carotid Artery

2014

Objective To analyze expression of keystone markers of apoptosis and the proapoptotic signaling pathway “unfolded protein response” (UPR) in rupture-prone plaques of the human carotid artery. Methods Plaque specimens were obtained during endarterectomy for high-grade carotid stenosis, and were formalin-fixed. Ten specimens were identified that exhibited criteria of advanced rupture-prone atherosclerotic plaques, and histological and immunohistological analysis of markers of apoptosis (cleaved Caspase-3, TUNEL) and UPR (KDEL, ATF3, CHOP, CHAC-1) was performed. In addition, co-localization of apoptosis and UPR-activation was assessed by double-immunohistochemistry. Results The mean size of th…

MalePathologymedicine.medical_specialtyReceptors PeptideArteriosclerosisKDELmedicine.medical_treatmentApoptosisCHOPImmunoenzyme TechniquesRisk FactorsIn Situ Nick-End LabelingMedicineHumansCarotid StenosisEndarterectomyAgedAtherosclerotic plaqueAged 80 and overMedicine(all)Endarterectomy CarotidTUNEL assayActivating Transcription Factor 3business.industryCaspase 3MacrophagesFibrous capMiddle AgedImmunohistochemistrymedicine.anatomical_structureCarotid ArteriesApoptosisUnfolded protein responseUnfolded Protein ResponseImmunohistochemistrySurgeryFemalebusinessCardiology and Cardiovascular MedicineBiomarkersTranscription Factor CHOPSignal TransductionEuropean Journal of Vascular and Endovascular Surgery
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Neuroprotection of lipoic acid treatment promotes angiogenesis and reduces the glial scar formation after brain injury

2012

After trauma brain injury, a large number of cells die, releasing neurotoxic chemicals into the extracellular medium, decreasing cellular glutathione levels and increasing reactive oxygen species that affect cell survival and provoke an enlargement of the initial lesion. Alpha-lipoic acid is a potent antioxidant commonly used as a treatment of many degenerative diseases such as multiple sclerosis or diabetic neuropathy. Herein, the antioxidant effects of lipoic acid treatment after brain cryo-injury in rat have been studied, as well as cell survival, proliferation in the injured area, gliogenesis and angiogenesis. Thus, it is shown that newborn cells, mostly corresponded with blood vessels …

MaleProgrammed cell deathAngiogenesisBlotting WesternNeovascularization PhysiologicPharmacologyBiologyNeuroprotectionAntioxidantsGlial scarNeovascularizationLesionCicatrixchemistry.chemical_compoundMicroscopy Electron TransmissionIn Situ Nick-End LabelingmedicineAnimalsRats WistarChromatography High Pressure LiquidGliogenesisThioctic AcidGeneral NeuroscienceImmunohistochemistryRatsLipoic acidNeuroprotective AgentschemistryBrain Injuriesmedicine.symptomNeurogliaNeuroscienceNeuroscience
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Cell death and oxidative stress in gliomas.

1999

In gliomas, apoptosis and necrosis are determined by a number of promoting and inhibiting factors including oxidative cell stress mediated by nitric oxide synthases (NOS) and reduced by superoxide dismutases. Therefore, in 46 gliomas (including astrocytomas, oligodendrogliomas, oligo-astrocytomas, and glioblastomas), the relationship of apoptosis and necrosis and the expression of apoptosis-promoting (p53, bax, Fas, Fas-L) and inhibiting (bcl-2) factors as well as of different isoforms of NOS (NOSb, NOSe, NOSi) and manganese superoxide dismutase (MnSOD) were studied. Apoptosis was measured in situ by the TUNEL method while expression profiles of apoptosis-related and oxidative stress-associ…

MaleProgrammed cell deathHistologyNecrosisTissue FixationOligodendrogliomaDNA FragmentationBiologyAstrocytomamedicine.disease_causePathology and Forensic MedicineSuperoxide dismutaseDownregulation and upregulationPhysiology (medical)GliomamedicineIn Situ Nick-End LabelingHumansAgedParaffin EmbeddingCell DeathBrain NeoplasmsCarcinomaGliomaMiddle Agedmedicine.diseaseImmunohistochemistrynervous system diseasesOxidative StressNeurologyApoptosisbiology.proteinCancer researchFemaleNeurology (clinical)Oligodendrogliomamedicine.symptomGlioblastomaOxidative stressNeuropathology and applied neurobiology
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Regulation of X-Chromosome-Linked Inhibitor of Apoptosis Protein in Kainic Acid-Induced Neuronal Death in the Rat Hippocampus

2001

XIAP (X-chromosome-linked inhibitor of apoptosis protein) is an antiapoptotic protein which inhibits the activity of caspases and suppresses cell death. However, little is known about the presence and function of XIAP in the nervous system. Here we report that XIAP mRNA is expressed in developing and adult rat brain. Using a specific antibody, we observed XIAP-immunoreactive cells in different brain regions, among others, in the hippocampus and cerebral cortex. Kainic acid, which induces delayed cell death of specific neurons, increased the levels of XIAP in the CA3 region of hippocampus. XIAP was, however, largely absent in cells undergoing cell death, as shown by TUNEL labeling and staini…

MaleProgrammed cell deathKainic acidX ChromosomeGenetic LinkageHippocampusApoptosisX-Linked Inhibitor of Apoptosis ProteinCaspase 3Hippocampal formationInhibitor of apoptosisHippocampusCellular and Molecular Neurosciencechemistry.chemical_compoundExcitatory Amino Acid AgonistsIn Situ Nick-End LabelingAnimalsRNA MessengerMolecular BiologyCells CulturedCaspaseNeuronsKainic AcidCell DeathbiologyCaspase 3Gene Expression Regulation DevelopmentalProteinsCell BiologyMolecular biologyRatsXIAPnervous systemchemistryCaspasesNerve Degenerationbiology.proteinBiomarkersMolecular and Cellular Neuroscience
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Histological and genetic studies in patients with bicuspid aortic valve and ascending aorta complications.

2011

OBJECTIVES: Aneurysm diameter and growing rate does not represent a definite parameter for operation in bicuspid aortic valve (BAV), ascending aortic aneurysm and normal root patients. Thus, we investigated histological and immunohistochemical aspects of different segments of ascending aorta (precisely, aortic root without dilatation, aneurysmatic tubular portion, dissected ascending aorta) and genetic features of patients with BAV and ascending aorta complication (aneurysm or dissection). METHODS: Aorta tissue samples of 24 BAV patients were examined. The patients comprised of 18 men and 6 women; the mean age was 54.2 ± 14.3 years. All patients underwent composite aortic root replacement (…

MalePulmonary and Respiratory MedicineAortic valveGenotypeBicuspid aortic valveHeart Valve DiseasesAorta ThoracicApoptosisPolymerase Chain ReactionPolymorphism Single NucleotideAortic aneurysmAneurysmBicuspid aortic valveRisk Factorsmedicine.arteryAscending aortaIn Situ Nick-End LabelingmedicineHumansThoracic aortaSettore MED/05 - Patologia ClinicaGenetic Predisposition to DiseaseCystRetrospective StudiesAortaAortic Aneurysm Thoracicbusiness.industryDissectionSettore MED/23 - Chirurgia CardiacaFollow-up PapersDNAAnatomyMiddle Agedmedicine.diseaseImmunohistochemistryAneurysmEchocardiography Doppler ColorAortic Dissectionmedicine.anatomical_structureAortic Valvecardiovascular systemFemaleSurgeryCardiology and Cardiovascular MedicinebusinessBiomarkersEchocardiography TransesophagealFollow-Up Studies
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Retinal oxidation, apoptosis and age- and sex-differences in the mnd mutant mouse, a model of neuronal ceroid lipofuscinosis

2004

Retinal degeneration is an early and progressive event in many forms of neuronal ceroid lipofuscinoses (NCLs), a heterogeneous group of neurodegenerative disorders with unknown pathogenesis. We here used the mutant motor neuron degeneration (mnd) mouse, a late-infantile NCL variant, to investigate the retinal oxidative state and apoptotic cell death as a function of age and sex. Total superoxide dismutase (SOD) activities and thiobarbituric acid-reactive substance (TBARS) levels revealed progressive increases in retinal oxyradicals and lipid peroxides of mnd mice of both sexes. Female mnd retinas showed a higher oxidation rate and consistently exhibited the 4-hydroxy-2-nonenal (4-HNE)-adduc…

MaleRetinal degenerationPathologymedicine.medical_specialtyApoptosisBiologymedicine.disease_causeThiobarbituric Acid Reactive SubstancesRetinaMiceMice Neurologic Mutantschemistry.chemical_compoundSex FactorsNeuronal Ceroid-LipofuscinosesIn Situ Nick-End LabelingmedicineAnimalsOuter nuclear layerMolecular BiologyAldehydesRetinaTUNEL assayLipid peroxideCaspase 3Superoxide DismutaseGeneral NeuroscienceRetinal DegenerationRetinalmedicine.diseaseImmunohistochemistryEnzyme ActivationMice Inbred C57BLDisease Models AnimalOxidative Stressmedicine.anatomical_structureBiochemistrychemistryCaspasesFemaleNeuronal ceroid lipofuscinosisNeurology (clinical)Oxidation-ReductionOxidative stressDevelopmental BiologyBrain Research
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Increase in Bcl-2 phosphorylation and reduced levels of BH3-only Bcl-2 family proteins in kainic acid-mediated neuronal death in the rat brain.

2003

Kainic acid induces excitotoxicity and nerve cell degeneration in vulnerable regions of rat brain, most markedly in hippocampus and amygdala. Part of the cell death following kainic acid is apoptotic as shown by caspase 3 activation and chromatin condensation. Here we have studied the regulation of pro- and anti-apoptotic proteins belonging to the Bcl-2 family in rat hippocampus and amygdala by kainic acid in relationship to ensuing neuronal death. The pro-apoptotic protein Bax was up-regulated in hippocampus 6 h after kainic acid administration. The increase in Bax was followed by the appearance of TdT-mediated dUTP nick end labelling-positive cells which were prominent at 24 h. Immunohist…

MaleTime FactorsExcitotoxicityCell Countmedicine.disease_causeSettore BIO/09 - Fisiologiachemistry.chemical_compoundPrecipitin TestExcitatory Amino Acid AgonistsSerinePhosphorylationCells CulturedNuclear Proteinbcl-2-Associated X ProteinNeuronsProto-Oncogene ProteinKainic AcidbiologyCell DeathImmunochemistryGeneral NeuroscienceBrainNuclear ProteinsImmunohistochemistryProto-Oncogene Proteins c-bcl-2Programmed cell deathKainic acidTime FactorNeuronal deathExcitatory Amino Acid AgonistBlotting WesternCaspase 3HippocampuBcl-2-associated X proteinProto-Oncogene ProteinsGlial Fibrillary Acidic ProteinmedicineIn Situ Nick-End LabelingAnimalsRats WistarProtein kinase AStaining and LabelingAnimalBcl-2 familyNeuronButylated HydroxytolueneEmbryo MammalianMolecular biologyPrecipitin Testsnervous system diseasesRatsnervous systemchemistrybiology.proteinRatNeuNBcl-2 proteinThe European journal of neuroscience
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Pregnenolone sulfate, a naturally occurring excitotoxin involved in delayed retinal cell death.

2002

The present study was designed to investigate the neurosteroid pregnenolone sulfate (PS), known for its ability to modulate NMDA receptors and interfere with acute excitotoxicity, in delayed retinal cell death. Three hours after exposure of the isolated and intact retina to a 30-min PS pulse, DNA fragmentation as assessed by genomic DNA gel electrophoresis and a modified in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method appeared concurrently with an increase in superoxide dismutase (SOD) activity and thiobarbituric acid-reactive substances (TBARS) levels. At 7 h, the increased amount of DNA laddering was accompanied by a higher number of TUN…

Malemedicine.medical_specialtyNeurotoxinsExcitotoxicityApoptosisDNA FragmentationDNA ladderingBiologymedicine.disease_causeBiochemistryReceptors N-Methyl-D-AspartateThiobarbituric Acid Reactive SubstancesRetinaCellular and Molecular Neurosciencechemistry.chemical_compoundAdjuvants ImmunologicSuperoxidesInternal medicinemedicineTBARSIn Situ Nick-End LabelingAnimalsCycloheximideRats WistarProgesteroneProtein Synthesis InhibitorsTUNEL assayEstradiolL-Lactate DehydrogenaseDehydroepiandrosterone SulfateSuperoxide DismutaseRatsEndocrinologychemistryApoptosisPregnenolonePregnenoloneDNA fragmentationLipid PeroxidationPregnenolone sulfateReactive Oxygen Speciesmedicine.drugJournal of neurochemistry
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