Search results for "Mitochondrial permeability transition pore"

showing 10 items of 23 documents

Effect of an Ilex paraguariensis (yerba mate) extract on infarct size in isolated rat hearts: the mechanisms involved

2016

Tea made from Ilex paraguariensis (IP) dried and minced leaves is a beverage widely consumed by large populations in South America as a source of caffeine (stimulant action) and for its medicinal properties. However, there is little information about the action of IP on the myocardium in the ischemia-reperfusion condition. Therefore, the objective of this study was to examine the effects of an aqueous extract of IP on infarct size in a model of regional ischemia. Isolated rat hearts were perfused by the Langendorff technique and subjected to 40 min of coronary artery occlusion followed by 60 min of reperfusion (ischemic control hearts). Other hearts received IP 30 μg mL-1 during the first 1…

0301 basic medicineMaleCIENCIAS MÉDICAS Y DE LA SALUDThiobarbituric acidIschemiaInmunologíaMyocardial InfarctionPharmacologyIn Vitro TechniquesIlex Paraguariensis03 medical and health scienceschemistry.chemical_compoundfoodIlex paraguariensisYerba-mateTBARSMedicineAnimalsHumansRats WistarIschemia-Reperfusionbiologybusiness.industryPlant ExtractsMyocardiumHeartGeneral MedicineGlutathione//purl.org/becyt/ford/3.1 [https]medicine.diseaseGlutathionefood.foodRatsNitric oxide synthaseMedicina Básica030104 developmental biologyMitochondrial permeability transition poreBiochemistrychemistrybiology.protein//purl.org/becyt/ford/3 [https]Nitric Oxide SynthasebusinessCaffeineFood Science
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Attenuation of 7-ketocholesterol- and 7β-hydroxycholesterol-induced oxiapoptophagy by nutrients, synthetic molecules and oils: Potential for the prev…

2021

Age-related diseases for which there are no effective treatments include cardiovascular diseases; neurodegenerative diseases such as Alzheimer's disease; eye disorders such as cataract and age-related macular degeneration; and, more recently, Severe Acute Respiratory Syndrome (SARS-CoV-2). These diseases are associated with plasma and/or tissue increases in cholesterol derivatives mainly formed by auto-oxidation: 7-ketocholesterol, also known as 7-oxo-cholesterol, and 7β-hydroxycholesterol. The formation of these oxysterols can be considered as a consequence of mitochondrial and peroxisomal dysfunction, leading to increased in oxidative stress, which is accentuated with age. 7-ketocholester…

0301 basic medicineProgrammed cell deathAgingOxysterolMitochondrionPharmacologymedicine.disease_causeBiochemistry03 medical and health sciences0302 clinical medicineLysosomemedicineHumansMolecular BiologyKetocholesterolsChemistrySARS-CoV-2COVID-19NutrientsPeroxisomeHydroxycholesterols030104 developmental biologymedicine.anatomical_structureNeurologyMitochondrial permeability transition poreEye disorderlipids (amino acids peptides and proteins)Oils030217 neurology & neurosurgeryOxidative stressBiotechnologyAgeing research reviews
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Hsp60 Post-translational Modifications: Functional and Pathological Consequences.

2020

Hsp60 is a chaperone belonging to the Chaperonins of Group I and typically functions inside mitochondria in which, together with the co-chaperonin Hsp10, maintains protein homeostasis. In addition to this canonical role, Hsp60 plays many others beyond the mitochondria, for instance in the cytosol, plasma-cell membrane, extracellular space, and body fluids. These non-canonical functions include participation in inflammation, autoimmunity, carcinogenesis, cell replication, and other cellular events in health and disease. Thus, Hsp60 is a multifaceted molecule with a wide range of cellular and tissue locations and functions, which is noteworthy because there is only one hsp60 gene. The questio…

0301 basic medicinechaperoninnon-canonical functionsReviewMitochondrioncanonical functionsBiochemistry Genetics and Molecular Biology (miscellaneous)Biochemistrychaperonopathies03 medical and health sciences0302 clinical medicineUbiquitinMolecular Bioscienceslcsh:QH301-705.5Molecular Biologybiologycanonical functions chaperonin Hsp60 non-canonical functions post-translation modificationChemistryfungiCitrullinationCell cycleHsp60Cell biology030104 developmental biologylcsh:Biology (General)Mitochondrial permeability transition pore030220 oncology & carcinogenesisChaperone (protein)biology.proteinPhosphorylationHSP60post-translation modificationFrontiers in molecular biosciences
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Down-regulation of OPA1 alters mouse mitochondrial morphology, PTP function, and cardiac adaptation to pressure overload

2012

AIMS: The optic atrophy 1 (OPA1) protein is an essential protein involved in the fusion of the mitochondrial inner membrane. Despite its high level of expression, the role of OPA1 in the heart is largely unknown. We investigated the role of this protein in Opa1(+/-) mice, having a 50% reduction in OPA1 protein expression in cardiac tissue. METHODS AND RESULTS: In mutant mice, cardiac function assessed by echocardiography was not significantly different from that of the Opa1(+/+). Electron and fluorescence microscopy revealed altered morphology of the Opa1(+/-) mice mitochondrial network; unexpectedly, mitochondria were larger with the presence of clusters of fused mitochondria and altered c…

Cardiac function curveendocrine systemPhysiologyAdaptation BiologicalDown-RegulationBiologyMitochondrionMitochondrial Membrane Transport ProteinsPermeabilityGTP PhosphohydrolasesMitochondrial ProteinsMice03 medical and health sciencesMitochondrial membrane transport protein0302 clinical medicinePhysiology (medical)Optic Atrophy Autosomal DominantPressuremedicineAnimalsMyocyteMyocytes CardiacInner mitochondrial membrane030304 developmental biologyMice KnockoutPressure overload0303 health sciencesMitochondrial Permeability Transition Poremedicine.diseaseeye diseasesMitochondriaCell biologyBiochemistryMitochondrial permeability transition poreMitochondrial Membranesbiology.proteinOptic Atrophy 1Cardiology and Cardiovascular Medicine030217 neurology & neurosurgeryCardiovascular Research
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Induction of apoptosis by arachidonic acid in human retinoblastoma Y79 cells: involvement of oxidative stress

2000

Arachidonic acid administration caused apoptosis in Y79 cells, as shown by typical morphological changes, phosphatidylserine externalization, chromatin condensation, processing and activation of caspase-3 and cleavage of the endogenous caspase substrate poly-(ADP-ribose)-polymerase. Arachidonic acid also caused lamin B cleavage, suggesting caspase-6 activation. Arachidonic acid treatment was accompanied by increased formation of the lipid peroxidation end products malondialdehyde and 4-hydroxy-2-nonenal, lowering in reduced glutathione content and in mitochondrial membrane potential. Inhibiting glutathione synthesis sensitized Y79 cells to apoptosis-inducing stimuli, whilst replenishing red…

Cell SurvivalBlotting WesternApoptosisCell Countmedicine.disease_causeMembrane PotentialsLipid peroxidationCellular and Molecular Neurosciencechemistry.chemical_compoundPhospholipase A2medicineTumor Cells Culturedarachidonic acidHumansCYP2C8biologyDose-Response Relationship DrugRetinoblastomaGlutathioneTrypan BlueMalondialdehydeFlow CytometryGlutathioneSensory SystemsCell biologyMitochondriaOphthalmologyOxidative StressBiochemistrychemistryMitochondrial permeability transition poreCaspasesbiology.proteinArachidonic acidColorimetryPoly(ADP-ribose) PolymerasesOxidative stress
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Ex Vivo Treatment with a Polyphenol-Enriched Cocoa Extract Ameliorates Myocardial Infarct and Postischemic Mitochondrial Injury in Normotensive and H…

2016

Our objective was to determine the effects of a polyphenol-enriched cocoa extract (PCE) on myocardial postischemic alterations in normotensive (Wistar rats, W) and spontaneously hypertensive rats (SHR). Isolated hearts were submitted to 110 min of perfusion or 20 min stabilization, 30 min global ischemia, and 60 min reperfusion (R). Other hearts were treated with PCE at the onset of R. Infarct size, the reduced glutathione (GSH), and the expression of phospho-Akt, P-GSK-3β, and P-eNOS were assessed. In isolated mitochondria, the Ca2+-mediated response of mitochondrial permeability transition pore (mPTP), membrane potential (δψm), and superoxide production were determined. PCE decreased infa…

Male0301 basic medicineMyocardial InfarctionWistarBlood Pressure030204 cardiovascular system & hematologyPharmacologyMitochondrial Membrane Transport ProteinsInfarct sizeSHRGlycogen Synthase Kinase 3chemistry.chemical_compound0302 clinical medicineMITOCHONDRIAIschemiaSuperoxidesEnosRats Inbred SHRbiologySuperoxideMPTPINFARCT SIZEHeart//purl.org/becyt/ford/3.1 [https]GlutathioneMitochondriaMedicina BásicaHypertension//purl.org/becyt/ford/3 [https]General Agricultural and Biological SciencesPerfusionCocaCardiotonic AgentsCIENCIAS MÉDICAS Y DE LA SALUDInmunologíaIschemiaIn Vitro Techniques03 medical and health sciencesPOLYPHENOLSWISTARmedicineAnimalsHumansRats WistarSHR; Wistar; infarct size; mitochondria; polyphenolsMitochondrial Permeability Transition PorePlant ExtractsMyocardiumCocoa ExtractPolyphenolsGeneral ChemistryGlutathionemedicine.diseasebiology.organism_classificationRats030104 developmental biologychemistryMitochondrial permeability transition poreCiencias MédicasJournal of Agricultural and Food Chemistry
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Investigating and re-evaluating the role of glycogen synthase kinase 3 beta kinase as a molecular target for cardioprotection by using novel pharmaco…

2019

Aims Glycogen synthase kinase 3 beta (GSK3β) link with the mitochondrial Permeability Transition Pore (mPTP) in cardioprotection is debated. We investigated the role of GSK3β in ischaemia (I)/reperfusion (R) injury using pharmacological tools. Methods and results Infarct size using the GSK3β inhibitor BIO (6-bromoindirubin-3'-oxime) and several novel analogues (MLS2776-MLS2779) was determined in anaesthetized rabbits and mice. In myocardial tissue GSK3β inhibition and the specificity of the compounds was tested. The mechanism of protection focused on autophagy-related proteins. GSK3β localization was determined in subsarcolemmal (SSM) and interfibrillar mitochondria (IFM) isolated from Lang…

Male0301 basic medicinePhysiologyMyocardial InfarctionAutophagy-Related ProteinsMyocardial Reperfusion Injury030204 cardiovascular system & hematologyMitochondrionPharmacologyMitochondrial Membrane Transport ProteinsMitochondria HeartStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineReperfusion therapyPhysiology (medical)AnimalsMyocytes CardiacProtein Kinase InhibitorsGSK3BMice Knockoutchemistry.chemical_classificationCardioprotectionReactive oxygen speciesGlycogen Synthase Kinase 3 betaMolecular StructureMitochondrial Permeability Transition PoreChemistryKinaseMPTPIsolated Heart PreparationMice Inbred C57BLDisease Models Animal030104 developmental biologyMitochondrial permeability transition poreFemaleRabbitsCardiology and Cardiovascular MedicineCyclophilin DSignal TransductionCardiovascular Research
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Altered insulin pathway compromises mitochondrial function and quality control both in in vitro and in vivo model systems.

2021

Abstract Altered insulin signaling and insulin resistance are considered the link between Alzheimer's disease (AD) and metabolic syndrome. Here, by using an in vitro and an in vivo model, we investigated the relationship between these disorders focusing on neuronal mitochondrial dysfunction and mitophagy. In vitro Aβ insult induced the opening of mitochondrial permeability transition pore (mPTP), mitochondrial membrane potential (ΔΨm) loss, and apoptosis while insulin addition ameliorated these dysfunctions. The same alterations were detected in a 16 weeks of age mouse model of diet-induced obesity and insulin resistance. In addition, we detected an increase of fission related proteins and …

MaleAgingAmyloid beta-Peptidemedicine.medical_treatmentMetabolic diseasePINK1Insulin pathway Neurodegeneration Metabolic diseases Mitochondrion Mitophagy AgingMitochondrionDiet High-FatParkinNOMiceInsulin resistanceMetabolic DiseasesCell Line TumorMitophagymedicineAnimalsHumansInsulinMitochondrionNeurodegenerationMolecular BiologyAmyloid beta-PeptidesbiologyAnimalChemistryInsulinMitophagyCell Biologymedicine.diseaseCell biologyMitochondriaMice Inbred C57BLInsulin receptorMitochondrial permeability transition porebiology.proteinMolecular MedicineInsulin ResistanceInsulin pathwayHumanSignal TransductionMitochondrion
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Controlled reperfusion after hypothermic heart preservation inhibits mitochondrial permeability transition-pore opening and enhances functional recov…

2006

We investigated whether low-pressure reperfusion may attenuate postischemic contractile dysfunction, limits necrosis and apoptosis after a prolonged hypothermic ischemia, and inhibits mitochondrial permeability transition-pore (MPTP) opening. Isolated rats hearts ( n = 72) were exposed to 8 h of cold ischemia and assigned to the following groups: 1) reperfusion with low pressure (LP = 70 cmH2O) and 2) reperfusion with normal pressure (NP = 100 cmH2O). Cardiac function was assessed during reperfusion using the Langendorff model. Mitochondria were isolated, and the Ca2+resistance capacity (CRC) of the MPTP was determined. Malondialdehyde (MDA) production, caspase-3 activity, and cytochrome c …

MaleNecrosisPhysiologyIschemiaHeart preservationMyocardial IschemiaMyocardial ReperfusionPharmacologyBiologyMitochondrionMitochondrial Membrane Transport ProteinsMitochondria HeartPermeabilityHypothermia InducedPhysiology (medical)MalondialdehydemedicinePressureAnimalsRats WistarCaspase 3Mitochondrial Permeability Transition PoreMyocardiumCytochromes cRecovery of Functionmedicine.diseaseFunctional recoveryRatsMitochondrial permeability transition poreApoptosisAnesthesiaCalciummedicine.symptomCardiology and Cardiovascular MedicineAmerican journal of physiology. Heart and circulatory physiology
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First Evidence for a Crosstalk Between Mitochondrial and NADPH Oxidase-Derived Reactive Oxygen Species in Nitroglycerin-Triggered Vascular Dysfunction

2008

Chronic nitroglycerin treatment results in development of nitrate tolerance associated with endothelial dysfunction (ED). We sought to clarify how mitochondria- and NADPH oxidase (Nox)-derived reactive oxygen species (ROS) contribute to nitrate tolerance and nitroglycerin-induced ED. Nitrate tolerance was induced by nitroglycerin infusion in male Wistar rats (100 microg/h/4 day) and in C57/Bl6, p47(phox/) and gp91(phox/) mice (50 microg/h/4 day). Protein and mRNA expression of Nox subunits were unaltered by chronic nitroglycerin treatment. Oxidative stress was determined in vascular rings and mitochondrial fractions of nitroglycerin-treated animals by L-012 enhanced chemiluminescence, revea…

MalePhysiologyVasodilator AgentsClinical BiochemistryMitochondrionPharmacologymedicine.disease_causeBiochemistryMitochondria HeartMiceNitroglycerinchemistry.chemical_compoundEthidiumAortaChromatography High Pressure LiquidHeart metabolismGeneral Environmental Sciencechemistry.chemical_classificationNADPH oxidasebiologyReverse Transcriptase Polymerase Chain ReactionReactive Nitrogen SpeciesBiochemistryCyclosporinecardiovascular systemcirculatory and respiratory physiologyBlotting WesternIn Vitro TechniquesTransfectionCell LineRotenonemedicineAnimalsHumansRNA MessengerRats WistarMolecular BiologyReactive oxygen speciesNADPH OxidasesCell BiologyRotenoneRatsMice Inbred C57BLchemistryMitochondrial permeability transition poreVasoconstrictionApocyninbiology.proteinGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidative stressAntioxidants & Redox Signaling
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