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showing 10 items of 14693 documents

Cholesterol Hydroxylating Cytochrome P450 46A1: From Mechanisms of Action to Clinical Applications

2021

Cholesterol, an essential component of the brain, and its local metabolism are involved in many neurodegenerative diseases. The blood-brain barrier is impermeable to cholesterol; hence, cholesterol homeostasis in the central nervous system represents a balance betweenin situbiosynthesis and elimination. Cytochrome P450 46A1 (CYP46A1), a central nervous system-specific enzyme, converts cholesterol to 24-hydroxycholesterol, which can freely cross the blood-brain barrier and be degraded in the liver. By the dual action of initiating cholesterol efflux and activating the cholesterol synthesis pathway, CYP46A1 is the key enzyme that ensures brain cholesterol turnover. In humans and mouse models,…

0301 basic medicineAgingCognitive Neuroscience24-hydroxycholesterolbrain[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyCentral nervous systemNeurosciences. Biological psychiatry. NeuropsychiatryReview03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineneurodegenerative diseasesAmyotrophic lateral sclerosisLipid raftlipid raftsbiologyCholesterolbusiness.industryphosphorylation[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyCytochrome P450cholesterolmedicine.diseaseplasma membranes3. Good healthVesicular transport proteinCYP46A1030104 developmental biologymedicine.anatomical_structurechemistrySpinocerebellar ataxiabiology.proteinAnimal studiesbusinessNeuroscience030217 neurology & neurosurgeryNeuroscienceRC321-571
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Targeting Nitric Oxide with Natural Derived Compounds as a Therapeutic Strategy in Vascular Diseases

2016

Within the family of endogenous gasotransmitters, nitric oxide (NO) is the smallest gaseous intercellular messenger involved in the modulation of several processes, such as blood flow and platelet aggregation control, essential to maintain vascular homeostasis. NO is produced by nitric oxide synthases (NOS) and its effects are mediated by cGMP-dependent or cGMP-independent mechanisms. Growing evidence suggests a crosstalk between the NO signaling and the occurrence of oxidative stress in the onset and progression of vascular diseases, such as hypertension, heart failure, ischemia, and stroke. For these reasons, NO is considered as an emerging molecular target for developing therapeutic stra…

0301 basic medicineAgingPhytochemicalsIschemiaEndogenyReview Article030204 cardiovascular system & hematologyPharmacologyBiologyNitric Oxidemedicine.disease_causeCardiovascular SystemBiochemistryNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineAnimalsHumansVascular Diseasescell biology; aging; biochemistrylcsh:QH573-671GasotransmittersPlants Medicinallcsh:CytologyPolyphenolsCardiovascular AgentsCell BiologyGeneral Medicinemedicine.diseaseDietOxidative StressCrosstalk (biology)030104 developmental biologychemistryHeart failurePlant PreparationsOxidative stressIntracellularPhytotherapySignal TransductionOxidative Medicine and Cellular Longevity
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Targeting the Endoplasmic Reticulum Unfolded Protein Response to Counteract the Oxidative Stress-Induced Endothelial Dysfunction

2017

In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production and antioxidant response can induce endothelial dysfunction, the initial event of many cardiovascular diseases. Recent studies have revealed that the endoplasmic reticulum could be a new player in the promotion of the pro- or antioxidative pathways and that in such a modulation, the unfolded protein response (UPR) pathways play an essential role. The UPR consists of a set of conserved signalling pathways evolved to restore the proteostasis during protein misfolding within the endoplasmic reticulum. Although the first outcome of the U…

0301 basic medicineAgingProgrammed cell deathendocrine systemOxidative phosphorylationReview Articlemedicine.disease_causeEndoplasmic ReticulumBiochemistryINITIATION-FACTOR 2-ALPHA03 medical and health sciencesProgrammed cell-deathSELECTIVE-INHIBITIONProgrammed cell-death;TXNIP/NLRP3 INFLAMMASOME ACTIVATION; MITOCHONDRIAL ELECTRON-TRANSPORT; SPONTANEOUSLY HYPERTENSIVE-RATS; INITIATION-FACTOR 2-ALPHA; CORONARY-ARTERY FUNCTION; ER STRESS; SELECTIVE-INHIBITION; MESSENGER-RNA; TRANSMEMBRANE PROTEINmedicineHumansEndothelial dysfunctionlcsh:QH573-671TXNIP/NLRP3 INFLAMMASOME ACTIVATIONSPONTANEOUSLY HYPERTENSIVE-RATSEndothelial Cellbusiness.industrylcsh:CytologyEndoplasmic reticulumfungiEndothelial CellsOxidative StreCell BiologyGeneral MedicineAdaptive responseMITOCHONDRIAL ELECTRON-TRANSPORTER STRESSmedicine.diseaseCell biologyOxidative Stress030104 developmental biologyProteostasisTRANSMEMBRANE PROTEINUnfolded protein responseUnfolded Protein ResponsebusinessMESSENGER-RNAOxidative stressCORONARY-ARTERY FUNCTIONHumanOxidative Medicine and Cellular Longevity
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Intensified mitophagy in skeletal muscle with aging is downregulated by PGC-1alpha overexpression in vivo.

2018

Mitochondrial dysfunction plays an important role in the etiology of age-related muscle atrophy known as sarcopenia. PGC-1α is positioned at the center of crosstalk in regulating mitochondrial quality control, but its role in mitophagy in aged skeletal muscle is currently unclear. The present study investigated the effects of aging and PGC-1α overexpression via in vivo DNA transfection on key mitophagy protein markers, as well as mitochondrial dynamics related proteins, metabolic function and antioxidant capacity in mouse muscle. C57BL/6J mice at the age of 2 mo (young, Y; N = 14) and 24 mo (old, O; N = 14) were transfected in vivo with either PGC-1α DNA (OE, N = 7) or GFP (N = 7) into the …

0301 basic medicineAgingUbiquitin-Protein LigasesPINK1MitochondrionBiochemistryMitochondrial DynamicsGTP Phosphohydrolases03 medical and health sciencesMice0302 clinical medicineIn vivoPhysiology (medical)MitophagymedicineAnimalsMuscle SkeletalChemistryMitophagySkeletal muscleTransfectionmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMuscle atrophyCell biologyMitochondriaOxidative Stress030104 developmental biologymedicine.anatomical_structureGene Expression RegulationSarcopeniaBeclin-1medicine.symptomProtein Kinases030217 neurology & neurosurgeryFree radical biologymedicine
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Biological and biophysics aspects of metformin-induced effects: cortex mitochondrial dysfunction and promotion of toxic amyloid pre-fibrillar aggrega…

2016

The onset of Alzheimer disease (AD) is influenced by several risk factors comprising diabetes. Within this context, antidiabetic drugs, including metformin, are investigated for their effect on AD. We report that in the C57B6/J mice, metformin is delivered to the brain where activates AMP-activated kinase (AMPK), its molecular target. This drug affects the levels of β- secretase (BACE1) and β-amyloid precursor protein (APP), promoting processing and aggregation of β-amyloid (Aβ), mainly in the cortex region. Moreover, metformin induces mitochondrial dysfunction and cell death by affecting the level and conformation of Translocase of the Outer Membrane 40 (TOM40), voltage-dependent anion-sel…

0301 basic medicineAgingmedicine.medical_specialtyMitochondrial poreAmyloidTranslocase of the outer membraneContext (language use)AMP-Activated Protein KinasesBiologyAmyloid beta-Protein PrecursorMice03 medical and health sciences0302 clinical medicineβ-amyloid aggregationAlzheimer DiseaseHexokinaseInternal medicine?-amyloid aggregationmitochondrial dysfunctionmedicineAnimalsHypoglycemic Agentsmitochondrial poresMitochondrial transportAmyloid beta-PeptidesVoltage-Dependent Anion Channel 1BrainAMPKcell degenerationCell BiologyAlzheimer's diseasemedicine.diseaseMitochondriaMetformin030104 developmental biologyEndocrinologyAmyloid Precursor Protein SecretasesAlzheimer's diseasemetforminVDAC1030217 neurology & neurosurgeryResearch Papermedicine.drug
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Estrogenic regulation of skeletal muscle proteome : a study of premenopausal women and postmenopausal MZ cotwins discordant for hormonal therapy

2017

Female middle age is characterized by a decline in skeletal muscle mass and performance, predisposing women to sarcopenia, functional limitations, and metabolic dysfunction as they age. Menopausal loss of ovarian function leading to low circulating level of 17b-estradiol has been suggested as a contributing factor to aging-related muscle deterioration. However, the underlying molecular mechanisms remain largely unknown and thus far androgens have been considered as a major anabolic hormone for skeletal muscle. We utilized muscle samples from 24 pre- and postmenopausal women to establish proteome-wide profiles, associated with the difference in age (30–34 years old vs. 54– 62 years old), men…

0301 basic medicineAgingnaisetlabel‐free protein quantitationProteomeAnabolismvaihdevuodetmedicine.medical_treatmentTwinsmenopausenano‐LC‐HD‐MSElihakset0302 clinical medicineSTRENGTHBRAIN315 Sport and fitness sciencesta315luustoINHIBITORHormone replacement therapy (menopause)ta3142MITOCHONDRIAL BIOGENESISMiddle AgedPostmenopauseMenopauseREPLACEMENThormone replacement therapyEditorialmedicine.anatomical_structurehormonihoitoHormonal therapyOriginal ArticleFemalemuscleswomenAdultestrogeenitnano-LC-HD-MSEEXPRESSIONmedicine.medical_specialtyBiologyestrogenic regulation03 medical and health sciencesmitochondrial functionInternal medicinemedicineHumansMuscle Skeletallabel-free protein quantitationmuscle proteomeAgedSkeletal muscleEstrogenslabel-free proteinquantitationOriginal ArticlesCell Biologyfunctional annotationmedicine.diseaseMiddle ageMONOZYGOTIC TWIN PAIRS030104 developmental biologyEndocrinologyPremenopauselihasmassaSarcopeniaCELLS3111 BiomedicineEnergy Metabolismfemale muscle030217 neurology & neurosurgeryskeletal musclesHormone
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Longevity-related molecular pathways are subject to midlife “switch” in humans

2019

Emerging evidence indicates that molecular aging may follow nonlinear or discontinuous trajectories. Whether this occurs in human neuromuscular tissue, particularly for the noncoding transcriptome, and independent of metabolic and aerobic capacities, is unknown. Applying our novel RNA method to quantify tissue coding and long noncoding RNA (lncRNA), we identified ~800 transcripts tracking with age up to ~60 years in human muscle and brain. In silico analysis demonstrated that this temporary linear “signature” was regulated by drugs, which reduce mortality or extend life span in model organisms, including 24 inhibitors of the IGF‐1/PI3K/mTOR pathway that mimicked, and 5 activators that oppos…

0301 basic medicineAgingved/biology.organism_classification_rank.speciesMuscle Fibers SkeletallihaksetTranscriptome0302 clinical medicineGene expressionGene Regulatory NetworksRNA-Seqmedia_commonCerebral CortexNeuronsreactive oxygen speciesihoTOR Serine-Threonine Kinasesmitochondrial complex 1LongevityBrainNon-coding RNAAlzheimer'sECSITCell biologytranskriptio (biologia)mTORRNA Long NoncodingOriginal ArticleaivotSignal TransductionAdultTranscriptional ActivationskinIn silicomedia_common.quotation_subjectLongevityBiology03 medical and health sciencesHumanslong noncoding RNAskeletal muscleModel organismGeneSirolimusved/biologyagingRNACell BiologyTwins MonozygoticOriginal Articles030104 developmental biologyikääntyminenRNATranscriptome030217 neurology & neurosurgery
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Sodium functions as a negative allosteric modulator of the oxytocin receptor

2017

Abstract The oxytocin receptor, a class A G protein coupled receptor (GPCR), is essentially involved in the physiology of reproduction. Two parameters are crucially important to support high-affinity agonist binding of the receptor: Mg2+ and cholesterol, both acting as positive modulators. Using displacement assays with a high-affinity fluorescent antagonist (OTAN-A647), we now show that sodium functions as a negative allosteric modulator of the oxytocin receptor. In membranes from HEK293 cells stably expressing the oxytocin receptor, oxytocin binding occurred with about 15-fold lower affinity when sodium chloride was increased from 0 to 300 mM, whereas antagonist binding remained largely u…

0301 basic medicineAgonistAllosteric modulatormedicine.drug_classSodiumBiophysicschemistry.chemical_elementBreast NeoplasmsSodium ChlorideOxytocinBiochemistryPotassium Chloride03 medical and health sciencesAllosteric RegulationCell Line TumormedicineHumansAmino Acid SequenceReceptorFluorescent DyesG protein-coupled receptorDose-Response Relationship DrugSequence Homology Amino AcidChemistryCell MembraneCell BiologyOxytocin receptorRecombinant ProteinsCell biologyCholesterolHEK293 Cells030104 developmental biologyOxytocinReceptors OxytocinMutagenesis Site-DirectedCalciumFemaleSequence Alignmenthormones hormone substitutes and hormone antagonistsIntracellularProtein Bindingmedicine.drugBiochimica et Biophysica Acta (BBA) - Biomembranes
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Transferability of PCR-based diagnostic protocols: An international collaborative case study assessing protocols targeting the quarantine pine pathog…

2019

Producción Científica

0301 basic medicineAgricultural BiotechnologyPerformanceInternational Cooperation1ST REPORTlcsh:Medicinediagnostica PCR protocolli PCR trasferibilità patologia forestale patogeni fungini fusarium circinatum malattie emergenti / PCR diagnostics protocol transferability emerging tree diseases fungal forest pathogensPolymerase Chain ReactionPine pitch cankerlaw.invention0302 clinical medicineFusariumlawChancro resinoso del pinoFalse positive paradoxDNA Fungallcsh:SciencePathogenPolymerase chain reactionPinus radiataEnfermedades fúngicas - DiagnósticoMultidisciplinaryAgricultural SciencesCausal agentPathogenic fungusPitch Canker disease3. Good healthOther Agricultural SciencesTests PCRGibberella-CircinataFusariumPolymerase-Chain-ReactionDNA PlantPlantationsBOTANICATransferabilityFusarium circinatumBiologyPitch cankerno key wordsReal-Time Polymerase Chain ReactionSensitivity and SpecificityArticleREAL-TIME PCR; POLYMERASE-CHAIN-REACTION; PITCH CANKER DISEASE; CAUSAL AGENT; GIBBERELLA-CIRCINATA; 1ST REPORT; QUANTIFICATION; SUSCEPTIBILITY; PLANTATIONS; PERFORMANCE03 medical and health sciencesGibberella circinataQuantificationQuarantineDiagnóstico de enfermedad fungicaFalse Positive ReactionsFungal infections - DiagnosisMolecular BiologyPlant DiseasesInvasive speciesbusiness.industrylcsh:RReproducibility of ResultsPinusbiology.organism_classificationPCR-based testsBiotechnology030104 developmental biology3106 Ciencia ForestalSusceptibilitylcsh:QReal-Time PCRbusinessPCR-based techniques030217 neurology & neurosurgeryScientific Reports
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ALCOHOLIC LIVER DISEASE: A MOUSE MODEL REVEALS PROTECTION BY LACTOBACILLUS FERMENTUM

2016

Objectives Alcoholism is one of the most devastating diseases with high incidence, but knowledge of its pathology and treatment is still plagued with gaps mostly because of the inherent limitations of research with patients. We developed an animal model for studying liver histopathology, Hsp (heat-shock protein)-chaperones involvement, and response to treatment. Methods The system was standardized using mice to which ethanol was orally administered alone or in combination with Lactobacillus fermentum following a precise schedule over time and applying, at predetermined intervals, a battery of techniques (histology, immunohistochemistry, western blotting, real-time PCR, immunoprecipitation, …

0301 basic medicineAlcoholic liver diseasePathologymedicine.medical_specialtyLactobacillus fermentumOriginal ContributionsPharmacologylaw.invention03 medical and health sciencesProbioticLiver diseaselawFibrosismedicineSettore BIO/06 - Anatomia Comparata E Citologiaprobiotics lactobacillus fermentum alcoholic liver diesease HspSettore MED/12 - Gastroenterologiabiologybusiness.industryGastroenterologymedicine.diseasebiology.organism_classificationNitric oxide synthase030104 developmental biologybiology.proteinImmunohistochemistrySteatosisbusiness
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