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showing 10 items of 11910 documents

Effect of chronic exercise on myocardial electrophysiological heterogeneity and stability. Role of intrinsic cholinergic neurons: A study in the isol…

2018

[EN] A study has been made of the effect of chronic exercise on myocardial electrophysiological heterogeneity and stability, as well as of the role of cholinergic neurons in these changes. Determinations in hearts from untrained and trained rabbits on a treadmill were performed. The hearts were isolated and perfused. A pacing electrode and a recording multielectrode were located in the left ventricle. The parameters determined during induced VF, before and after atropine (1 mu M), were: fibrillatory cycle length (VV), ventricular functional refractory period (FRPVF), normalized energy (NE) of the fibrillatory signal and its coefficient of variation (CV), and electrical ventricular activatio…

0301 basic medicineAtropineMaleRefractory Period ElectrophysiologicalRefractory periodPhysiology030204 cardiovascular system & hematologyBiochemistryRunningTissue Culture Techniques0302 clinical medicineAnimal CellsMuscarinic acetylcholine receptorMedicine and Health SciencesMedicinePublic and Occupational HealthTreadmillMammalsNeuronsMultidisciplinaryQREukaryotaHeartNeurochemistryNeurotransmittersAnimal ModelsSports ScienceCardiovascular physiologyElectrophysiologyAtropineChemistrymedicine.anatomical_structureExperimental Organism SystemsVentricular FibrillationPhysical SciencesVertebratesCardiologyLeporidsMedicineRabbitsCellular TypesAnatomyArrhythmiamedicine.drugResearch Articlemedicine.medical_specialtyScienceCholinergicsCardiologyMuscarinic AntagonistsResearch and Analysis MethodsTECNOLOGIA ELECTRONICA03 medical and health sciencesAlkaloidsInternal medicineAnimalsCholinergic neuronSports and Exercise MedicineExercisebusiness.industryChemical CompoundsOrganismsParasympatholyticsBiology and Life SciencesCell BiologyPhysical ActivityElectrophysiology030104 developmental biologyVentriclePhysical FitnessCellular NeuroscienceAmniotesAnimal StudiesCardiovascular AnatomybusinessNeuroscience
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Mitochondrial bioenergetic pathways in blood leukocyte transcriptome decrease after intensive weight loss but are rescued following weight regain in …

2021

Prolonged periods of energy deficit leading to weight loss induce metabolic adaptations resulting in reduced energy expenditure, but the mechanisms for energy conservation are incompletely understood. We examined 42 healthy athletic females (age 27.5 +/- 4.0 years, body mass index 23.4 +/- 1.7 kg/m(2)) who volunteered into either a group dieting for physique competition (n = 25) or a control group (n = 17). The diet group substantially reduced their energy intake and moderately increased exercise levels to induce loss of fat mass that was regained during a voluntary weight regain period. The control group maintained their typical lifestyle habits and body mass as instructed. From the diet g…

0301 basic medicineBioenergeticsWeight GainruokavaliotBiochemistryTranscriptomeravitsemuskäyttäytyminen0302 clinical medicineWeight lossaineenvaihdunta2. Zero hungerexerciseAdaptation PhysiologicalMitochondriaFemalemedicine.symptomenergiankulutus (aineenvaihdunta)fyysinen aktiivisuusBiotechnologyDietingAdultmedicine.medical_specialtyleukocytesmitokondriotoxidative phosphorylationBiologypainonnousuribosomesYoung Adult03 medical and health sciencesInternal medicineWeight LossGeneticsmedicineMetabolomeHumansMolecular Biologyitsensä johtaminenlaihdutusAMPKMetabolism030104 developmental biologyEndocrinologyenergiansaanti1182 Biochemistry cell and molecular biologylihavuus3111 BiomedicineEnergy IntakeTranscriptomedietBody mass index030217 neurology & neurosurgery
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Cardiolipin synthesis in brown and beige fat mitochondria is essential for systemic energy homeostasis

2018

Summary Activation of energy expenditure in thermogenic fat is a promising strategy to improve metabolic health, yet the dynamic processes that evoke this response are poorly understood. Here we show that synthesis of the mitochondrial phospholipid cardiolipin is indispensable for stimulating and sustaining thermogenic fat function. Cardiolipin biosynthesis is robustly induced in brown and beige adipose upon cold exposure. Mimicking this response through overexpression of cardiolipin synthase (Crls1) enhances energy consumption in mouse and human adipocytes. Crls1 deficiency in thermogenic adipocytes diminishes inducible mitochondrial uncoupling and elicits a nuclear transcriptional respons…

0301 basic medicineBiologiaBioenergeticsChop-10 ; Crls1 ; Beige Adipose ; Brown Adipose ; Cardiolipin ; Insulin Resistance ; Lipid Metabolism ; Mitochondria ; Phospholipids ; ThermogenesisPhysiologyGlucose uptakeAdipose tissueTransferases (Other Substituted Phosphate Groups)MitochondrionEnergy homeostasischemistry.chemical_compoundMice0302 clinical medicineAdipose Tissue Browninsulin resistancelipid metabolismCardiolipinAdipocytesCells CulturedThermogenesisthermogenesisCell biologyMitochondriamitochondriaCHOP-10lipids (amino acids peptides and proteins)BioquímicaCardiolipinsbeige adiposeArticle03 medical and health sciencesInsulin resistanceCRLS1medicineAnimalsHumansMolecular Biologyphospholipidsbrown adiposeMembrane ProteinsCell BiologyAdipose Tissue Beigemedicine.diseaseMice Inbred C57BL030104 developmental biologychemistrycardiolipinEnergy MetabolismThermogenesis030217 neurology & neurosurgery
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Polyphosphate as a metabolic fuel in Metazoa: A foundational breakthrough invention for biomedical applications

2015

In animals, energy-rich molecules like ATP are generated in the intracellular compartment from metabolites, e.g. glucose, taken up by the cells. Recent results revealed that inorganic polyphosphates (polyP) can provide an extracellular system for energy transport and delivery. These polymers of multiple phosphate units, linked by high-energy phosphoanhydride bonds, use blood platelets as transport vehicles to reach their target cells. In this review it is outlined how polyP affects cell metabolism. It is discussed that polyP influences cell activity in a dual way: (i) as a metabolic fuel transferring metabolic energy through the extracellular space; and (ii) as a signaling molecule that amp…

0301 basic medicineBiomedical TechnologyMitochondrionBiologyEndocytosisApplied Microbiology and Biotechnology03 medical and health scienceschemistry.chemical_compoundAdenosine TriphosphateTissue engineeringPolyphosphatesExtracellularHumansBlood CellsPolyphosphateGeneral MedicineCell biologyMitochondriaMetabolic pathway030104 developmental biologychemistryBiochemistryMolecular MedicineNanoparticlesAdenosine triphosphateIntracellularMetabolic Networks and PathwaysBiotechnology Journal
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Curcumin as a therapeutic option in retinal diseases

2020

Este artículo se encuentra disponible en la siguiente URL: https://www.mdpi.com/2076-3921/9/1/48 Este artículo pertenece al número especial "Natural products in health promotion and disease prevention". En este artículo también participa: Vincent M. Villar. The retina is subjected to oxidative stress due to its high vascularization, long time light exposition and a high density of mitochondria. Oxidative stress can lead to pathological processes, like cell apoptosis, angiogenesis and inflammation ending in retinal pathologies. Curcumin, a major bioactive component obtained from the spice turmeric (Curcuma longa) rhizome has been used for centuries in Asian countries for cooking and for curi…

0301 basic medicineBioquímicaretinaAntioxidantPhysiologyBioquímica clínicamedicine.medical_treatmentClinical BiochemistryCurcumina - Uso terapéutico.InflammationReviewPharmacologyMitochondrionmedicine.disease_causeBiochemistryRetina03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineoxidative stresscurcuminCurcumaMolecular BiologyVistachemistry.chemical_classificationEstrés oxidativo.Reactive oxygen speciesBiología molecularbiologybusiness.industryRetina - Diseases - Treatment.lcsh:RM1-950RetinalCell Biologybiology.organism_classificationCurcumin - Therapeutic use.Oxidative stress.030104 developmental biologylcsh:Therapeutics. Pharmacologyretinal diseaseschemistry030220 oncology & carcinogenesisCurcuminmedicine.symptombusinessCúrcumaOxidative stressRetina - Enfermedades - Tratamiento.
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Fine-Tuning of Platelet Responses by Serine/Threonine Protein Kinases and Phosphatases-Just the Beginning.

2021

AbstractComprehensive proteomic analyses of human and murine platelets established an extraordinary intracellular repertoire of signaling components, which control crucial functions. The spectrum of platelet serine/threonine protein kinases (more than 100) includes the AGC family (protein kinase A, G, C [PKA, PKG, PKC]), the mitogen-activated protein kinases (MAPKs), and others. PKA and PKG have multiple significantly overlapping substrates in human platelets, which possibly affect functions with clear “signaling nodes” of regulation by multiple protein kinases/phosphatases. Signaling nodes are intracellular Ca2+ stores, the contractile system (myosin light chains), and other signaling comp…

0301 basic medicineBlood PlateletsProteomicsThreonineMyosin Light ChainsPhosphataseSerine threonine protein kinase030204 cardiovascular system & hematology03 medical and health sciencesMice0302 clinical medicinePhosphoprotein PhosphatasesSerineAnimalsHumansSyk KinasePlatelet activationProtein kinase AProtein kinase CKinaseChemistryHematologyProtein phosphatase 2Platelet ActivationCell biology030104 developmental biologyModels AnimalMitogen-Activated Protein KinasesTyrosine kinaseProtein KinasesSignal TransductionHamostaseologie
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Sphingolipids and Inositol Phosphates Regulate the Tau Protein Phosphorylation Status in Humanized Yeast

2020

Hyperphosphorylation of protein tau is a hallmark of Alzheimer’s disease (AD). Changes in energy and lipid metabolism have been correlated with the late onset of this neurological disorder. However, it is uncertain if metabolic dysregulation is a consequence of AD or one of the initiating factors of AD pathophysiology. Also, it is unclear whether variations in lipid metabolism regulate the phosphorylation state of tau. Here, we show that in humanized yeast, tau hyperphosphorylation is stimulated by glucose starvation in coincidence with the downregulation of Pho85, the yeast ortholog of CDK5. Changes in inositol phosphate (IP) signaling, which has a central role in energy metabolism, altere…

0301 basic medicineCDK5Cèl·lulesTau proteinSit42HyperphosphorylationSaccharomyces cerevisiaeSACCHAROMYCES-CEREVISIAECeramide03 medical and health scienceschemistry.chemical_compoundCell and Developmental Biology0302 clinical medicineInositolceramideYpk1Inositol phosphatelcsh:QH301-705.51-IP7Original Researchchemistry.chemical_classificationScience & TechnologybiologyChemistryKinaseNEURODEGENERATIONLipid metabolismCell BiologyProtein phosphatase 2Fpk1MICROTUBULE-BINDINGPho85SERINE PALMITOYLTRANSFERASECell biologyALZHEIMERS-DISEASE030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesisGLYCOGEN-SYNTHASE KINASE-3-BETAbiology.proteinKINASE-ACTIVITYPhosphorylationLife Sciences & BiomedicineBETA TOXICITYProteïnesDevelopmental BiologyFrontiers in Cell and Developmental Biology
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IL4 Primes the Dynamics of Breast Cancer Progression via DUSP4 Inhibition

2017

Abstract The tumor microenvironment supplies proinflammatory cytokines favoring a permissive milieu for cancer cell growth and invasive behavior. Here we show how breast cancer progression is facilitated by IL4 secreted by adipose tissue and estrogen receptor–positive and triple-negative breast cancer cell types. Blocking autocrine and paracrine IL4 signaling with the IL4Rα antagonist IL4DM compromised breast cancer cell proliferation, invasion, and tumor growth by downregulating MAPK pathway activity. IL4DM reduced numbers of CD44+/CD24− cancer stem-like cells and elevated expression of the dual specificity phosphatase DUSP4 by inhibiting NF-κB. Enforced expression of DUSP4 drove conversio…

0301 basic medicineCancer ResearchBlotting WesternCA 15-3Breast Neoplasms03 medical and health sciencesParacrine signalling0302 clinical medicineBreast cancerCell Line TumorTumor MicroenvironmentmedicineHumansskin and connective tissue diseasesAutocrine signallingDual-Specificity PhosphataseBlotting Western; Breast Neoplasms; Cell Line Tumor; Disease Progression; Dual-Specificity Phosphatases; Female; Flow Cytometry; Heterografts; Humans; Interleukin-4; Mitogen-Activated Protein Kinase Phosphatases; Tumor Microenvironment; Oncology; Cancer ResearchTumor microenvironmentbiologyCD44CancerFlow Cytometrymedicine.disease030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyCancer cellDisease Progressionbiology.proteinCancer researchDual-Specificity PhosphatasesHeterograftsMitogen-Activated Protein Kinase PhosphatasesFemaleInterleukin-4HeterograftMitogen-Activated Protein Kinase PhosphataseBreast NeoplasmHumanCancer Research
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Oxidative stress preconditioning of mouse perivascular myogenic progenitors selects a subpopulation of cells with a distinct survival advantage in vi…

2018

AbstractCell engraftment, survival and integration during transplantation procedures represent the crux of cell-based therapies. Thus, there have been many studies focused on improving cell viability upon implantation. We used severe oxidative stress to select for a mouse mesoangioblast subpopulation in vitro and found that this subpopulation retained self-renewal and myogenic differentiation capacities while notably enhancing cell survival, proliferation and migration relative to unselected cells. Additionally, this subpopulation of cells presented different resistance and recovery properties upon oxidative stress treatment, demonstrating select advantages over parental mesoangioblasts in …

0301 basic medicineCancer ResearchCellular differentiationCellstem cells; oxidative stress; clone isolation/dk/atira/pure/subjectarea/asjc/2800/2804Mice SCIDp38 Mitogen-Activated Protein KinasesMiceCell MovementProtein IsoformsMuscular Dystrophy/dk/atira/pure/subjectarea/asjc/2400/2403Settore BIO/06 - Anatomia Comparata E Citologiaeducation.field_of_studylcsh:CytologyStem CellsSettore BIO/13Cell DifferentiationSkeletalCell biologymedicine.anatomical_structureMuscleMatrix Metalloproteinase 2Animals; Cell Cycle Checkpoints; Cell Differentiation; Cell Line; Cell Movement; Cell Survival; Hydrogen Peroxide; Matrix Metalloproteinase 2; Mice; Mice SCID; Muscle Skeletal; Muscular Dystrophy Animal; Oxidative Stress; Protein Isoforms; Reactive Oxygen Species; Sarcoglycans; Stem Cell Transplantation; Stem Cells; p38 Mitogen-Activated Protein Kinases/dk/atira/pure/subjectarea/asjc/1300/1306/dk/atira/pure/subjectarea/asjc/1300/1307Cell SurvivalPopulationImmunologyBiologySCIDArticleCell Line03 medical and health sciencesCellular and Molecular NeuroscienceIn vivoSarcoglycansmedicineAnimalsProgenitor celllcsh:QH573-671educationMuscle Skeletaloxidative streMesoangioblastAnimalCell BiologyCell Cycle CheckpointsHydrogen PeroxideMuscular Dystrophy Animalclone isolationTransplantationstem cellOxidative Stress030104 developmental biologyCell cultureReactive Oxygen SpeciesStem Cell TransplantationCell Death & Disease
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PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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