Search results for "HOS"

showing 10 items of 15105 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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Adult rat myelin enhances axonal outgrowth from neural stem cells.

2018

Axon regeneration after spinal cord injury (SCI) is attenuated by growth inhibitory molecules associated with myelin. We report that rat myelin stimulated the growth of axons emerging from rat neural progenitor cells (NPCs) transplanted into sites of SCI in adult rat recipients. When plated on a myelin substrate, neurite outgrowth from rat NPCs and from human induced pluripotent stem cell (iPSC)-derived neural stem cells (NSCs) was enhanced threefold. In vivo, rat NPCs and human iPSC-derived NSCs extended greater numbers of axons through adult central nervous system white matter than through gray matter and preferentially associated with rat host myelin. Mechanistic investigations excluded …

0301 basic medicineAgingNeuronalNudeMessengerNeurodegenerativeInbred C57BLRegenerative MedicineMedical and Health SciencesMyelinMiceNeural Stem CellsStem Cell Research - Nonembryonic - HumanCyclic AMPAxonPhosphorylationGray MatterInduced pluripotent stem cellExtracellular Signal-Regulated MAP KinasesSpinal Cord InjuryMyelin SheathInbred F344Neuronal growth regulator 1Stem Cell Research - Induced Pluripotent Stem Cell - HumanChemistryGeneral MedicineBiological SciencesWhite MatterNeural stem cellCell biologymedicine.anatomical_structureSpinal Cord5.1 PharmaceuticalsNeurologicalFemaleStem Cell Research - Nonembryonic - Non-HumanDevelopment of treatments and therapeutic interventionsPhysical Injury - Accidents and Adverse EffectsNeuriteCell Adhesion Molecules NeuronalCentral nervous systemNeuronal OutgrowthArticleWhite matter03 medical and health sciencesRats NudemedicineAnimalsHumansRNA MessengerStem Cell Research - Embryonic - HumanTraumatic Head and Spine InjuryTransplantationStem Cell Research - Induced Pluripotent Stem CellNeurosciencesStem Cell ResearchRats Inbred F344AxonsRatsMice Inbred C57BL030104 developmental biologynervous systemChondroitin Sulfate ProteoglycansRNACell Adhesion Molecules
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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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Overexpression of glucose 6 phosphate dehydrogenase preserves mouse pancreatic beta cells function until late in life.

2021

NAD(P)H donates electrons for reductive biosynthesis and antioxidant defense across all forms of life. Glucose-6- phosphate dehydrogenase (G6PD) is a critical enzyme to provide NADPH. G6PD deficiency is present in more than 400 million people worldwide. This enzymopathy provides protection against malaria but sensitizes cells to oxidative stressors. Oxidative stress has been involved in the pathogenesis of the diabetic complications and several studies have provided evidences of a link between G6PD deficiency and type 2 diabetes (T2D). We hypothesized that a moderate overexpression of G6PD (G6PD-Tg) could protect β-cells from age-associated oxidative stress thus reducing the risk of develop…

0301 basic medicineAgingmedicine.medical_specialtyOxidative phosphorylationType 2 diabetesGlucosephosphate Dehydrogenasemedicine.disease_causeBiochemistry03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinehemic and lymphatic diseasesPhysiology (medical)Internal medicineDiabetes mellitusInsulin-Secreting Cellsparasitic diseasesNADPHmedicineGlucose-6-phosphate dehydrogenaseAnimalsPancreatic isletsDiabetesWild typenutritional and metabolic diseasesmedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologymedicine.anatomical_structureGlucosephosphate Dehydrogenase DeficiencychemistryDiabetes Mellitus Type 2Oxidative stressPancreas030217 neurology & neurosurgeryOxidative stressFree radical biologymedicine
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Effects of intrinsic aerobic capacity, aging and voluntary running on skeletal muscle sirtuins and heat shock proteins

2016

Aim Sirtuins are proteins that connect energy metabolism, oxidative stress and aging. Expression of heat shock proteins (Hsps) is regulated by heat shock factors (HSFs) in response to various environmental and physiological stresses, such as oxidative stress. Oxidative stress accumulates during aging which makes cells more prone to DNA damage. Although many experimental animal models have been designed to study the effects of knockdown or overexpression of sirtuins, HSFs and Hsps, little is known about how aging per se affects their expression. Here we study the impact of intrinsic aerobic capacity, aging and voluntary exercise on the levels of sirtuins, HSFs and Hsps in skeletal muscle. Me…

0301 basic medicineAgingmedicine.medical_specialtyphysical activityCitrate (si)-SynthaseOxidative phosphorylationta3111medicine.disease_causeBiochemistryRunning03 medical and health sciences0302 clinical medicineEndocrinologyPhysical Conditioning AnimalHeat shock proteinInternal medicineGeneticsmedicineAnimalsSirtuinsAerobic exerciseta318skeletal muscleta315Muscle Skeletaloksidatiivinen stressiMolecular BiologyHeat-Shock ProteinsAerobic capacitybiologyagingBody WeightSkeletal muscleRats Inbred StrainsCell BiologyHsp70sirtuinOxidative Stress030104 developmental biologymedicine.anatomical_structureEndocrinologySirtuinbiology.proteinFemaleEnergy Intake030217 neurology & neurosurgeryOxidative stressExperimental Gerontology
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Abacavir Increases Purinergic P2X7 Receptor Activation by ATP: Does a Pro-inflammatory Synergism Underlie Its Cardiovascular Toxicity?

2021

16 p.-9 fig.-1 tab.

0301 basic medicineAgonistAllosteric modulatormedicine.drug_classAllosteric modulatoradenosine triphosphateAllosteric regulationPharmacologyleukocyte-endothelium interactionsProinflammatory cytokine03 medical and health scienceschemistry.chemical_compound0302 clinical medicineimmune system diseasesAbacavirmedicinePharmacology (medical)Original ResearchPharmacologyApyraseLeukocyte-endothelium interactionsabacavirlcsh:RM1-950Purinergic receptorallosteric modulatorvirus diseasesAbacavircardiovascular diseasesCardiovascular diseaseslcsh:Therapeutics. Pharmacology030104 developmental biologychemistryP2X7 receptorAdenosine triphosphate030217 neurology & neurosurgeryAdenosine triphosphatemedicine.drugFrontiers in Pharmacology
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Desensitization of cAMP Accumulation via Human β3-Adrenoceptors Expressed in Human Embryonic Kidney Cells by Full, Partial, and Biased Agonists

2019

β3-Adrenoceptors couple not only to cAMP formation but, at least in some cell types, also to alternative signaling pathways such as phosphorylation of extracellular signal-regulated kinase (ERK). β3-Adrenoceptor agonists are used in long-term symptomatic treatment of the overactive bladder syndrome; it is only poorly understood which signaling pathway mediates the clinical response and whether it undergoes agonist-induced desensitization. Therefore, we used human embryonic kidney cells stably transfected with human β3-adrenoceptors to compare coupling of ligands with various degrees of efficacy, including biased agonists, to cAMP formation and ERK phosphorylation, particularly regarding des…

0301 basic medicineAgonistMAPK/ERK pathwaymedicine.drug_classmedicine.medical_treatmentdesensitization03 medical and health scienceschemistry.chemical_compoundpartial agonism0302 clinical medicinecAMPIsoprenalinemedicinePharmacology (medical)β3-adrenoceptorOriginal ResearchDesensitization (medicine)PharmacologyForskolinKinaselcsh:RM1-950extracellular signal-related kinaseCell biologylcsh:Therapeutics. Pharmacology030104 developmental biologybiased agonismchemistry030220 oncology & carcinogenesisPhosphorylationSignal transductionmedicine.drugFrontiers in Pharmacology
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Postnatal development of the dopaminergic signaling involved in the modulation of intestinal motility in mice

2015

Background:Since antidopaminergic drugs are pharmacological agents employed in the management of gastrointestinal motor disorders at all ages, we investigated whether the enteric dopaminergic system may undergo developmental changes after birth.Methods:Intestinal mechanical activity was examined in vitro as changes in isometric tension.Results:In 2-d-old (P2) mice, dopamine induced a contractile effect, decreasing in intensity with age, replaced, at the weaning (day 20), by a relaxant response. Both responses were tetrodotoxin (TTX)-insensitive. In P2, dopaminergic contraction was inhibited by D1-like receptor antagonist and mimicked by D1-like receptor agonist. In 90-d-old (P90) mice, the …

0301 basic medicineAgonistmedicine.medical_specialtyGastrointestinal Diseasesmedicine.drug_classDopamineTetrodotoxinBiologySettore BIO/09 - FisiologiaEnteric Nervous SystemMice03 medical and health sciences0302 clinical medicineDopamine receptor D3DopamineInternal medicineIntestine SmallCyclic AMPmedicineAnimalsEstrenesReceptorDopaminergicReceptor antagonistPyrrolidinonesMice Inbred C57BL030104 developmental biologyEndocrinologyAnimals NewbornDopamine receptorType C PhospholipasesDideoxyadenosinePediatrics Perinatology and Child Health2345-Tetrahydro-78-dihydroxy-1-phenyl-1H-3-benzazepineSignal transductionGastrointestinal Motility030217 neurology & neurosurgerySignal Transductionmedicine.drugPediatric Research
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Refining the Baveno VI elastography criteria for the definition of compensated advanced chronic liver disease

2021

Background: The Baveno VI consensus proposed a dual liver stiffness (LS) by transient elastography threshold of <10 and >15 kPa for excluding and diagnosing compensated advanced chronic liver disease (cACLD) in the absence of other clinical signs. Herein, we aimed to validate these criteria in a real-world multicentre study. Methods: We included 5,648 patients (mean age 51 ± 13 years, 53% males) from 10 European liver centres who had a liver biopsy and LS measurement within 6 months. We included patients with chronic hepatitis C (n = 2,913, 52%), non-alcoholic fatty liver disease (NAFLD, n = 1,073, 19%), alcohol-related liver disease (ALD, n = 946, 17%) or chronic hepatitis B (n = 716…

0301 basic medicineAlcoholic liver diseasemedicine.medical_specialtyCirrhosis[SDV]Life Sciences [q-bio]Chronic liver diseaseAsymptomaticGastroenterology03 medical and health sciencesLiver disease0302 clinical medicineInternal medicineNAFLDmedicineViral hepatitis10. No inequalityPortal hypertensionComputingMilieux_MISCELLANEOUSCirrhosiHepatologymedicine.diagnostic_testbusiness.industryFatty liverAlcoholic liver diseasemedicine.disease3. Good health030104 developmental biologyFibroscanCirrhosisLiver biopsyFIB-4030211 gastroenterology & hepatologymedicine.symptomTransient elastographybusinessViral hepatitis.
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