Search results for "Downregulation"

showing 10 items of 460 documents

OGT and OGA expression in postmenopausal skeletal muscle associates with hormone replacement therapy and muscle cross-sectional area

2013

Protein glycosylation via O-linked N-acetylglucosaminylation (O-GlcNAcylation) is an important post-translational regulatory mechanism mediated by O-GlcNAc transferase (OGT) and responsive to nutrients and stress. OGT attaches an O-GlcNAc moiety to proteins, while O-GlcNAcase (OGA) catalyzes O-GlcNAc removal. In skeletal muscle of experimental animals, prolonged increase in O-GlcNAcylation associates with age and muscle atrophy. Here we examined the effects of hormone replacement therapy (HRT) and power training (PT) on muscle OGT and OGA gene expression in postmenopausal women generally prone to age-related muscle weakness. In addition, the associations of OGT and OGA gene expressions with…

medicine.medical_specialtyAgingGlycosylationTime Factorsmedicine.drug_classPlyometric ExerciseBiologyta3111N-AcetylglucosaminyltransferasesBiochemistryGene Expression Regulation EnzymologicEndocrinologyDownregulation and upregulationInternal medicineGene expressionGeneticsmedicineHumansMuscle StrengthRNA Messengerta315Muscle SkeletalMolecular BiologyFinlandGlyceraldehyde 3-phosphate dehydrogenasePlyometric power trainingEstrogen Replacement Therapyta1182Age FactorsMuscle weaknessSkeletal muscleta3141Cell BiologyMiddle Agedbeta-N-AcetylhexosaminidasesMuscle atrophyPostmenopausePhenotypeTreatment OutcomeEndocrinologymedicine.anatomical_structureEstrogenbiology.proteinFemaleMuscle atrophymedicine.symptomProtein Processing Post-TranslationalMuscle ContractionMuscle contraction
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PPAR in Cardiovascular Disorders

2016

Peroxisome proliferation-activated receptors (PPARs) are ligand-inducible transcription factors that, upon binding their ligands, translocate into the nucleus, where they regulate transcription of numerous genes that have the peroxisome proliferator response element (PPRE) in the promoter region [1]. In humans, there are 3 PPAR isoforms: PPAR-α, PPAR-β/δ, and PPAR-γ. The isoforms have partially overlapping spectra of activity and are differently expressed in organs and tissues [2]. PPAR-α is expressed mostly in tissues characterized by high catabolic activity, including skeletal muscle, liver, proximal tubular cells in kidneys, and brown fat. This PPAR isoform regulates components of β-oxid…

medicine.medical_specialtyArticle SubjectPeroxisome proliferator-activated receptor030209 endocrinology & metabolism030204 cardiovascular system & hematologyBiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationInternal medicineDrug DiscoverymedicineGlucose homeostasisPharmacology (medical)Beta oxidationlcsh:QH301-705.5chemistry.chemical_classificationFatty acid metabolismLipid metabolismPeroxisomeEndocrinologyEditorialchemistrylcsh:Biology (General)Rosiglitazonemedicine.drugPPAR Research
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Chronic aspartame intake causes deficient glutathione synthesis and induces cxcl1 up-regulation in mice liver

2018

Reduced glutathione (GSH) depletion and inflammation have been linked to chronic aspartame consumption. However, the cause of aspartame-induced GSH depletion and the role of pro- and anti-inflammatory cytokines in aspartame-triggered inflammation are still unknown. The aims of this research were to investigate if aspartame causes GSH depletion due to deficient synthesis and also which pro- and anti-inflammatory genes are involved in aspartame-related inflammation in mice liver. Mice were divided into three groups: control, aspartame (80 mg kg-1, v.o., 3 months), aspartame treated with N-acetylcysteine (NAC) (1 mmol kg-1, i.p., last month). Aspartame markedly reduced GSH, γ-glutamylcysteine …

medicine.medical_specialtyAspartameInflammationGlutathioneBiochemistryCXCL1chemistry.chemical_compoundGCLCEndocrinologychemistryDownregulation and upregulationPhysiology (medical)Internal medicineMolemedicinemedicine.symptomCysteineFree Radical Biology and Medicine
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Amphiregulin activates human hepatic stellate cells and is upregulated in non alcoholic steatohepatitis

2015

AbstractAmphiregulin (AR) involvement in liver fibrogenesis and hepatic stellate cells (HSC) regulation is under study. Non-alcoholic fatty liver disease (NAFLD) and its more severe form non-alcoholic steatohepatitis (NASH) may progress to cirrhosis and hepatocellular cancer (HCC). Our aim was to investigate ex vivo the effect of AR on human primary HSC (hHSC) and verify in vivo the relevance of AR in NAFLD fibrogenesis. hHSC isolated from healthy liver segments were analyzed for expression of AR and its activator, TNF-α converting enzyme (TACE). AR induction of hHSC proliferation and matrix production was estimated in the presence of antagonists. AR involvement in fibrogenesis was also ass…

medicine.medical_specialtyBiopsyGene ExpressionADAM17 ProteinBiologyAmphiregulinSeverity of Illness Indexp38 Mitogen-Activated Protein Kinasesdigestive systemArticleMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineDownregulation and upregulationAmphiregulinGrowth factor receptorNon-alcoholic Fatty Liver DiseaseInternal medicineHepatic Stellate CellsmedicineAnimalsHumansProtein Kinase CPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesMultidisciplinaryFatty livernutritional and metabolic diseasesmedicine.diseaseFibrosisActinsdigestive system diseases3. Good healthEnzyme ActivationErbB ReceptorsADAM ProteinsDisease Models AnimalEndocrinologyHepatic stellate cellCancer research030211 gastroenterology & hepatologyTumor necrosis factor alphaCollagenSteatohepatitisSignal TransductionScientific Reports
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From obesity to Alzheimer's disease through insulin resistance

2021

Alzheimer's disease is one of the most frequent forms of dementia. It is a progressive neurodegenerative disease, characterized by presence of amyloid plaques and neurofibrillary tangles in the brain. Obesity is regarded as abnormal fat accumulation with deleterious impact on human health. There is full scientific evidence that obesity and the metabolic comorbidities (e.g., insulin resistance, hyperglycaemia, and type 2 diabetes) are related to Alzheimer's disease and likely in the causative pathway. Numerous studies have identified several overlapping neurodegenerative mechanisms, including oxidative stress, mitochondrial dysfunction, and inflammation. In this review, we present how obesit…

medicine.medical_specialtyEndocrinology Diabetes and MetabolismType 2 diabetesmedicine.disease_causeEndocrinologyInsulin resistanceDownregulation and upregulationAlzheimer DiseaseInternal medicineDiabetes mellitusInternal MedicinemedicineHumansDementiaObesityNeurodegenerationInflammationbusiness.industryNeurodegenerationBrainInsulin resistanceAlzheimer's diseasemedicine.diseaseEndocrinologyDiabetes Mellitus Type 2LipotoxicitybusinessOxidative stressJournal of Diabetes and its Complications
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Aclidinium, a New Long-Acting Antimuscarinic, Inhibits Cholinergic and Cigarette Smoke-Induced Up Regulation of Mucin MUC5AC Expression in Human Airw…

2009

medicine.medical_specialtyEndocrinologyLong actingDownregulation and upregulationbusiness.industryInternal medicineMucinmedicineCholinergicCigarette smokeHuman airwayPharmacologybusiness
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Angiotensin II induces leukocyte-endothelial cell interactions in vivo via AT(1) and AT(2) receptor-mediated P-selectin upregulation.

2000

Background —Angiotensin II (Ang II) plays a critical role in the development of vascular lesions in hypertension, atherosclerosis, and several renal diseases. Because Ang II may contribute to the leukocyte recruitment associated with these pathological states, the aim of the present study was to assess the role of Ang II in leukocyte–endothelial cell interactions in vivo. Methods and Results —Intravital microscopy of the rat mesenteric postcapillary venules was used. Sixty minutes of superfusion with 1 nmol/L Ang II induced a significant increase in leukocyte rolling flux (83.8±20.7 versus 16.4±3.1 cells/min), adhesion (11.4±1.0 versus 0.8±0.5 cells/100 μm), and emigration (4.0±0.7 versus …

medicine.medical_specialtyEndotheliumPyridinesLeukocyte RollingCell CommunicationReceptor Angiotensin Type 2LosartanReceptor Angiotensin Type 1Rats Sprague-DawleyDownregulation and upregulationPhysiology (medical)Internal medicineCromolyn SodiummedicineLeukocytesAnimalsEndotheliumReceptorAngiotensin II receptor type 1Receptors Angiotensinbusiness.industryAngiotensin IIImidazolesFlow CytometryAngiotensin IIRatsUp-RegulationEndothelial stem cellP-Selectinmedicine.anatomical_structureEndocrinologyLosartanCardiology and Cardiovascular Medicinebusinessmedicine.drugCirculation
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Expression of different isoforms of nitric oxide synthase in experimentally denervated and reinnervated skeletal muscle.

1997

Denervated muscle fibers express enhanced levels of stress and apoptosis-associated proteins and undergo apoptosis. In experimentally denervated and reinnervated rat facial muscle, we now evaluate changes in the expression patterns of different isoforms of nitric oxide synthase (NOS)-generating nitric oxide (NO), which mediates oxidative stress and apoptosis. Physiological expression of NOS corresponds to a constant sarcolemmal staining pattern for neuronal NOS (nNOS) and a patchy sarcolemmal and weak sarcoplasmic labeling for the endothelial NOS-isoform, with no expression for inducible NOS (iNOS). Denervated muscle displayed distinct downregulation of nNOS with preserved expression of dys…

medicine.medical_specialtyEndotheliumSarcoplasmFacial MusclesPathology and Forensic MedicineNitric oxideCellular and Molecular Neurosciencechemistry.chemical_compoundDownregulation and upregulationReference ValuesInternal medicinemedicineAnimalsEndotheliumRats WistarDenervationbiologySkeletal muscleGeneral MedicineMuscle DenervationNerve RegenerationRatsNitric oxide synthaseIsoenzymesmedicine.anatomical_structureEndocrinologyNeurologychemistryEnzyme Inductionbiology.proteinFemaleNeurology (clinical)Nitric Oxide SynthaseDystrophinJournal of neuropathology and experimental neurology
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The impact of alpha1-adrenoceptors up-regulation accompanied by the impairment of beta-adrenergic vasodilatation in hypertension

2008

9 pages, 7 figures, 3 tables.-- PMID: 19060223 [PubMed]

medicine.medical_specialtyG-Protein-Coupled Receptor Kinase 2Adrenergic receptorSystolemedia_common.quotation_subjectAdrenergicVasodilationModels BiologicalRats Inbred WKYDownregulation and upregulationHeart RateRats Inbred SHRReceptors Adrenergic alpha-1Internal medicineReceptors Adrenergic betamedicineAnimalsHumansRNA MessengerReceptorInternalizationAortamedia_commonPharmacologybiologyChemistryKinaseBeta adrenergic receptor kinaseRatsUp-RegulationVasodilationEndocrinologyHypertensionbiology.proteinMolecular Medicine
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Developmental and tumoral vascularization is regulated by G protein-coupled receptor kinase 2

2012

Tumor vessel dysfunction is a pivotal event in cancer progression. Using an in vivo neovascularization model, we identified G protein–coupled receptor kinase 2 (GRK2) as a key angiogenesis regulator. An impaired angiogenic response involving immature vessels was observed in mice hemizygous for Grk2 or in animals with endothelium-specific Grk2 silencing. ECs isolated from these animals displayed intrinsic alterations in migration, TGF-β signaling, and formation of tubular networks. Remarkably, an altered pattern of vessel growth and maturation was detected in postnatal retinas from endothelium-specific Grk2 knockout animals. Mouse embryos with systemic or endothelium-selective Grk2 ablation …

medicine.medical_specialtyG-Protein-Coupled Receptor Kinase 2Angiogenic SwitchAngiogenesisMedicinaActivin Receptors Type IIMelanoma ExperimentalReceptor Transforming Growth Factor-beta Type INeovascularization PhysiologicProtein Serine-Threonine KinasesBiologyMural cellGrk2Transforming Growth Factor beta1NeovascularizationMiceDownregulation and upregulationCell MovementPregnancyInternal medicinemedicineAnimalsHumansCell ProliferationHemizygoteMice KnockoutG protein-coupled receptor kinaseTumorNeovascularization PathologicEndothelial CellsRetinal VesselsG proteinGeneral MedicineCell biologyEndocrinologymedicine.anatomical_structurecardiovascular systemFemalePericyteSignal transductionmedicine.symptomActivin Receptors Type IReceptors Transforming Growth Factor betaSignal TransductionResearch Article
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