Search results for "programme"

showing 10 items of 874 documents

Midgut pseudotumors and the maintenance of tissue homeostasis: studies on aging and manipulated stick insects.

2009

Stick insects (Carausius morosus) develop pseudotumors in aging adults. Pseudotumor formation starts at the M2 midgut region where an accumulation of stomatogastric nerve terminals is observed. Pseudotumors arise from dying columnar cells whose basal parts form an “amorphous substance” at the basement membrane whereas the apical parts, including the nucleus, are expelled into the gut lumen. The “amorphous substance” is ensheathed by hemocytes. These nodules, which do not melanize, characterize the phenotype of the pseudotumors. With age, cell death and pseudotumor infestation increases. It is shown that the maintenance of midgut tissue homoeostasis is disturbed and becomes more serious with…

Carausius morosusProgrammed cell deathPathologymedicine.medical_specialtyAgingInsectaMidgutColumnar CellBiologybiology.organism_classificationModels BiologicalGastrointestinal Tractstomatognathic diseasesStomatogastric nervous systemmedicineAnimalsHomeostasisAnimal Science and ZoologyStem cellHomeostasisTissue homeostasisDevelopmental BiologyJournal of morphology
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miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction

2014

Summary miR-133a and miR-1 are known as muscle-specific microRNAs that are involved in cardiac development and pathophysiology. We have shown that both miR-1 and miR-133a are early and progressively upregulated during in vitro cardiac differentiation of adult cardiac progenitor cells (CPCs), but only miR-133a expression was enhanced under in vitro oxidative stress. miR-1 was demonstrated to favor differentiation of CPCs, whereas miR-133a overexpression protected CPCs against cell death, targeting, among others, the proapoptotic genes Bim and Bmf. miR-133a-CPCs clearly improved cardiac function in a rat myocardial infarction model by reducing fibrosis and hypertrophy and increasing vasculari…

Cardiac function curveProgrammed cell deathMyocardial InfarctionGene ExpressionCardiomegalyBiologyBiochemistryArticleMuscle hypertrophyParacrine signallingDownregulation and upregulationmiR-133a; Cardiac Progenitors Cells; Myocardial InfarctionFibrosisREGENERATIONmicroRNAGeneticsmedicineMyocyteAnimalsRNA MessengerOXIDATIVE STRESSlcsh:QH301-705.5ENGINEERED HEART-TISSUElcsh:R5-920Gene Expression ProfilingMICRORNAComputational BiologyCell BiologyMUSCLEmedicine.disease3. Good healthCell biologyRatsAPOPTOSISHYPERTROPHYMicroRNAsDIFFERENTIATIONlcsh:Biology (General)ImmunologyGROWTHRNA Interferencelcsh:Medicine (General)EMBRYONIC STEM-CELLSMyoblasts CardiacDevelopmental BiologyStem Cell Reports
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Dystrophin-deficiency increases the susceptibility to doxorubicin-induced cardiotoxicity

2007

Background and aim: The clinical use of doxorubicin (DOX) and other anthracyclines is limited by a dosage-dependent cardiotoxicity, which can lead to cardiomyopathy. The role of the individual genetic makeup in this disorder is poorly understood. Alterations in genes encoding cardiac cytoskeleton or sarcolemma proteins may increase the susceptibility to doxorubicin-related cardiotoxicity. Methods: Female dystrophin-deficient mice (MDX) and age-matched wild-type mice underwent chronic treatment with doxorubicin. Cardiac function and tissue damage were assessed by echocardiography and histopathology, respectively. Gene expression changes were investigated using microarrays. Results: DOX treat…

Cardiac function curveProgrammed cell deathPathologymedicine.medical_specialtyHeart DiseasesCytoskeleton organizationCardiomyopathyGene Expression030204 cardiovascular system & hematologyDystrophinMice03 medical and health sciences0302 clinical medicineRisk FactorsmedicineAnimalsDoxorubicinUltrasonography030304 developmental biology0303 health sciencesCardiotoxicityAntibiotics AntineoplasticSarcolemmabiologybusiness.industryGenetic VariationMicroarray Analysismedicine.disease3. Good healthDoxorubicinDisease Progressionbiology.proteinCancer researchFemaleDisease SusceptibilityCardiology and Cardiovascular MedicineDystrophinbusinessmedicine.drugEuropean Journal of Heart Failure
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Abstract 4219: Lysosomal membrane permeabilization, a novel anticancer mechanism induced by pterostilbene

2011

Abstract Pterostilbene (Pter) (3,5-dimethoxy-4′-hydroxystilbene), a natural dimethylated analog of resveratrol, is a phytoalexin abundant in plants and fruits with a number of potential benefits for human health. Darakchasava, an Indian herbal preparation of Vitis Vinifera, contains Pter and is prescribed as a cardiotonic in ayurvedic and traditional medicine. Furthermore, some observations indicate that Pter can be beneficial in the prevention and treatment of different diseases such as diabetes, dyslipidemia, or cancer. Pter shows higher bioavailability than resveratrol. The substitution of two OH groups (positions 3 and 5) by methyl groups increases the stabilityof the molecule and its r…

CathepsinCancer ResearchProgrammed cell deathPterostilbenebiologyCaspase 3ResveratrolMolecular biologychemistry.chemical_compoundLysosomal lumenOncologyBiochemistrychemistryApoptosisbiology.proteinCaspaseCancer Research
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Characteristic ERK1/2 signaling dynamics distinguishes necroptosis from apoptosis

2021

International audience; ERK1/2 involvement in cell death remains unclear, although many studies have demonstrated the importance of ERK1/2 dynamics in determining cellular re- sponses. To untangle how ERK1/2 contributes to two cell death programs, we investigated ERK1/2 signaling dynamics during hFasL-induced apoptosis and TNF-induced necroptosis in L929 cells. We observed that ERK1/2 inhibition sensi- tizes cells to apoptosis while delaying necroptosis. By monitoring ERK1/2 activity by live-cell imaging using an improved ERK1/2 biosensor (EKAR4.0), we reported differential ERK1/2 signaling dynamics between cell survival, apoptosis, and nec- roptosis. We also decrypted a temporally shifted …

Cell biologyProgrammed cell deathScience[SDV]Life Sciences [q-bio]Necroptosis[SDV.BBM.BP] Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsPROTEINMECHANISMSESCRTACTIVATION03 medical and health sciences0302 clinical medicineINFLAMMATIONGene expressionMedicine and Health SciencesKINASEBiology030304 developmental biology0303 health sciencesMultidisciplinaryIDENTIFICATIONChemistryNECROSISQDynamics (mechanics)Biology and Life SciencesErk1 2 signalingCell biology[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biophysics[SDV] Life Sciences [q-bio]Biological sciencesBiomolecular engineeringCELL-DEATHApoptosisCell culture030220 oncology & carcinogenesisTumor necrosis factor alphaBIOSENSORSHuman medicineiScience
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The MDM2-p53 pathway is involved in preconditioning-induced neuronal tolerance to ischemia

2018

Brain preconditioning (PC) refers to a state of transient tolerance against a lethal insult that can be evoked by a prior mild event. It is thought that PC may induce different pathways responsible for neuroprotection, which may involve the attenuation of cell damage pathways, including the apoptotic cell death. In this context, p53 is a stress sensor that accumulates during brain ischemia leading to neuronal death. The murine double minute 2 gene (MDM2), a p53-specific E3 ubiquitin ligase, is the main cellular antagonist of p53, mediating its degradation by the proteasome. Here, we study the role of MDM2-p53 pathway on PC-induced neuroprotection both in cultured neurons (in vitro) and rat …

Cell death0301 basic medicineProgrammed cell deathCell SurvivalNeuronalScience2415 Biología MolecularIschemiaNeuroprotectionArticleBrain ischemiaMiceBrain ischemia03 medical and health sciences0302 clinical medicineIschemiaXarxes neuronals (Neurobiologia)medicineAnimalsIschemic PreconditioningCell damageCells CulturedBrain preconditioningNeuronsMultidisciplinarybiologyChemistryQRBrainProto-Oncogene Proteins c-mdm2MDM2-p53medicine.diseaseNeuroprotectionRatsCell biologyUbiquitin ligaseDisease Models Animal030104 developmental biology2490 Neurocienciasbiology.proteinMedicineIschemic preconditioningMdm2Tumor Suppressor Protein p53030217 neurology & neurosurgerySignal Transduction
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Central and Peripheral Secondary Cell Death Processes after Transient Global Ischemia in Nonhuman Primate Cerebellum and Heart

2019

Cerebral ischemia and its pathological sequelae are responsible for severe neurological deficits generally attributed to the neural death within the infarcted tissue and adjacent regions. Distal brain regions, and even peripheral organs, may be subject to more subtle consequences of the primary ischemic event which can initiate parallel disease processes and promote comorbid symptomology. In order to characterize the susceptibility of cerebellar brain regions and the heart to transient global ischemia (TGI) in nonhuman primates (NHP), brain and heart tissues were harvested 6 months post-TGI injury. Immunostaining analysis with unbiased stereology revealed significant cell death in lobule II…

Cell deathInflammationPathologymedicine.medical_specialtyProgrammed cell deathCerebellumbusiness.industryPurkinje cellNeurodegenerationIschemiaInflammationStereologymedicine.diseaseSecondary injury03 medical and health sciences0302 clinical medicinemedicine.anatomical_structureApoptosis030220 oncology & carcinogenesisMedicineNeurodegenerationmedicine.symptombusiness030217 neurology & neurosurgeryImmunostaining
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Onset of heart failure determines the hepatic cell death pattern.

2011

Background and rationale. Acute and chronic heart failure (HF) may affect the liver, but the underlying mechanisms that lead to progressive liver damage are poorly understood. The hepatic cytokeratin-18 (CK18) epitopes M65 and M30 have been reported to distinguish between overall (necrotic) and apoptotic cell death, respectively. We aimed to evaluate the predominant hepatic cell death pattern in acute vs. chronic heart failure and examined if these assays predict the course of the disease. Main results. In a prospective study comprising 21 patients with acute HF (AHF) and 18 patients with chronic HF (CHF) serum levels of M65 and M30 were assessed. Compared with CHF, M65 levels were signific…

Cell deathMalemedicine.medical_specialtyProgrammed cell deathMedizinM65Specialties of internal medicineApoptosisLiver injuryEpitopesPredictive Value of TestsInternal medicinemedicineHumansProspective StudiesProspective cohort studySurvival analysisHeart FailureLiver injuryKeratin-18HepatologyCytokeratin 18business.industryM30Liver DiseasesGeneral MedicineMiddle AgedPrognosismedicine.diseaseSurvival AnalysisRC581-951LiverApoptosisPredictive value of testsHeart failureAcute DiseaseChronic DiseaseHepatic stellate cellCardiologyFemalebusinessBiomarkers
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Human Hsp10 and Early Pregnancy Factor (EPF) and their relationship and involvement in cancer and immunity: current knowledge and perspectives.

2009

This article is about Hsp10 and its intracellular and extracellular forms focusing on the relationship of the latter with Early Pregnancy Factor and on their roles in cancer and immunity. Cellular physiology and survival are finely regulated and depend on the correct functioning of the entire set of proteins. Misfolded or unfolded proteins can cause deleterious effects and even cell death. The chaperonins Hsp10 and Hsp60 act together inside the mitochondria to assist protein folding. Recent studies demonstrated that these proteins have other roles inside and outside the cell, either together or independently of each other. For example, Hsp10 was found increased in the cytosol of different t…

Cell physiologyHsp10 tumor immunity chaperonins early pregnancy factor developmentProgrammed cell deathProtein Foldingmedicine.medical_treatmentBiologyPregnancy ProteinsGeneral Biochemistry Genetics and Molecular BiologyAutoimmune DiseasesImmune systemImmunityNeoplasmsExtracellularmedicineChaperonin 10Suppressor Factors ImmunologicHumansGeneral Pharmacology Toxicology and PharmaceuticsSettore BIO/16 - Anatomia UmanaGrowth factorGeneral MedicineCell biologyMitochondriaProtein TransportHSP60IntracellularLife sciences
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Resveratrol reduces oxidative stress and cell death and increases mitochondrial antioxidants and XIAP in PC6.3-cells.

2010

Resveratrol, a polyphenol derived e.g. from red grapes, has been shown to mediate several positive biological actions such as protection of cells against oxidative stress. It can also influence cell signaling, but the mechanisms behind its antioxidant properties are largely unknown. Here we show that RSV reduces oxidative stress and enhances cell survival in PC6.3 cells depending on the concentration. In these cells, RSV increased the levels of antioxidants, SOD2 and TRX2, and of X chromosome-linked inhibitor of apoptosis protein. RSV also activated NFκB signaling as shown using luciferase reporter constructs. These findings show that RSV regulates oxidative stress and mitochondrial antioxi…

Cell signalingProgrammed cell deathBlotting WesternSOD2Settore BIO/11 - Biologia MolecolareApoptosisX-Linked Inhibitor of Apoptosis ProteinMitochondrionBiologyResveratrolmedicine.disease_causeInhibitor of apoptosisSettore BIO/09 - FisiologiaPolymerase Chain ReactionAntioxidantsCell LineMitochondrial Proteins03 medical and health scienceschemistry.chemical_compoundXIAP0302 clinical medicineThioredoxinsStilbenesmedicineTRX2Humans030304 developmental biologyNeurons0303 health sciencesSuperoxide DismutaseGeneral Neurosciencefood and beveragesROSSOD23. Good healthXIAPCell biologyMitochondriaOxidative StressBiochemistrychemistryResveratrolSettore BIO/14 - FarmacologiaOxidative stre030217 neurology & neurosurgeryOxidative stressNFκBNeuroscience letters
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