Search results for "Growth factor"

showing 10 items of 1300 documents

Functional role of endothelial CXCL16/CXCR6-platelet-leucocyte axis in angiotensin II-associated metabolic disorders.

2018

Aims Angiotensin-II (Ang-II) is the main effector peptide of the renin-angiotensin system (RAS) and promotes leucocyte adhesion to the stimulated endothelium. Because RAS activation and Ang-II signalling are implicated in metabolic syndrome (MS) and abdominal aortic aneurysm (AAA), we investigated the effect of Ang-II on CXCL16 arterial expression, the underlying mechanisms, and the functional role of the CXCL16/CXCR6 axis in these cardiometabolic disorders. Methods and results Results from in vitro chamber assays revealed that CXCL16 neutralization significantly inhibited mononuclear leucocyte adhesion to arterial but not to venous endothelial cells. Flow cytometry and immunofluorescence s…

0301 basic medicineMaleRHOAPhysiologyMice Knockout ApoE030204 cardiovascular system & hematology0302 clinical medicineLeukocytesReceptorCells CulturedMetabolic SyndromebiologyChemistryAngiotensin IIMiddle AgedAortic AneurysmVascular endothelial growth factor ALosartanmedicine.anatomical_structurecardiovascular systemFemaleCardiology and Cardiovascular Medicinemedicine.drugSignal TransductionAdultBlood Plateletsmedicine.medical_specialtyEndothelium03 medical and health sciencesPhysiology (medical)Internal medicinemedicineCell AdhesionAnimalsHumansPlatelet activationReceptors CXCR6Angiotensin II receptor type 1Endothelial CellsChemokine CXCL16Platelet ActivationAngiotensin IICoculture TechniquesMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyCase-Control Studiesbiology.proteinAngiotensin II Type 1 Receptor BlockersCardiovascular research
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Mutations in SKI in Shprintzen-Goldberg syndrome lead to attenuated TGF-β responses through SKI stabilization.

2020

ABSTRACTShprintzen-Goldberg syndrome (SGS) is a multisystemic connective tissue disorder, with considerable clinical overlap with Marfan and Loeys-Dietz syndromes. These syndromes have commonly been associated with enhanced TGF-β signaling. In SGS patients, heterozygous point mutations have been mapped to the transcriptional corepressor SKI, which is a negative regulator of TGF-β signaling that is rapidly degraded upon ligand stimulation. The molecular consequences of these mutations, however, are not understood. Here we use a combination of structural biology, genome editing and biochemistry to show that SGS mutations in SKI abolish its binding to phosphorylated SMAD2 and SMAD3. This resul…

0301 basic medicineMaleSMADmedicine.disease_causeMarfan SyndromeActivin0302 clinical medicineGenome editingTransforming Growth Factor betaGene expressionBiology (General)MutationShprintzen-Goldberg syndromeGeneral NeuroscienceQRShprintzen–Goldberg syndromeGeneral MedicineLigand (biochemistry)Chromosomes and Gene ExpressionCell biologyDNA-Binding ProteinsMedicinePhosphorylationFemaleSignal TransductionResearch ArticleHumanTGF-βQH301-705.5ScienceBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCraniosynostosesstomatognathic systemBiochemistry and Chemical BiologyProto-Oncogene ProteinsmedicineHumansGeneral Immunology and MicrobiologyPoint mutationmedicine.diseaseSKIArachnodactyly030104 developmental biologyStructural biologyMutation030217 neurology & neurosurgerySMADTransforming growth factoreLife
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VEGF-B gene therapy inhibits doxorubicin-induced cardiotoxicity by endothelial protection

2016

Congestive heart failure is one of the leading causes of disability in long-term survivors of cancer. The anthracycline antibiotic doxorubicin (DOX) is used to treat a variety of cancers, but its utility is limited by its cumulative cardiotoxicity. As advances in cancer treatment have decreased cancer mortality, DOX-induced cardiomyopathy has become an increasing problem. However, the current means to alleviate the cardiotoxicity of DOX are limited. We considered that vascular endothelial growth factor-B (VEGF-B), which promotes coronary arteriogenesis, physiological cardiac hypertrophy, and ischemia resistance, could be an interesting candidate for prevention of DOX-induced cardiotoxicity …

0301 basic medicineMaleVEGFBVascular Endothelial Growth Factor BAnthracyclineAdipose Tissue WhiteCardiomyopathyheart failureApoptosisheart030204 cardiovascular system & hematologyPharmacologyta3111Mitochondria Heart03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorNeoplasmsmedicinepolycyclic compoundscancerAnimalsDoxorubicinTube formationCardiotoxicityMultidisciplinaryAntibiotics Antineoplasticbusiness.industryta1184MyocardiumEndothelial CellsGenetic TherapyBiological Sciencesmedicine.diseaseCardiotoxicity3. Good healthVascular endothelial growth factorMice Inbred C57BL030104 developmental biologychemistryLiverDoxorubicinHeart failureendothelial cellArteriogenesisbusinessmedicine.drugDNA Damage
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Biomarkers for vascular ageing in aorta tissues and blood samples.

2019

Abstract Objectives Functional and quantitative alterations and senescence of circulating and expanded endothelial progenitor cells (EPC), as well as systemic and tissue modifications of angiogenetic and inflammatory molecules, were evaluated for predicting age-related vessel wall remodeling, correlating them to intima media thickness (IMT) in the common carotid artery (CCA), a biomarker of early cardiovascular disease and aortic root dilation. Populations and methods A homogenous Caucasian population was included in the study, constituted by 160 healthy subjects (80 old subjects, mean age 72 ± 6.4, range 66–83 years; and 80 younger blood donors, mean age 26.2 ± 3.4, range 21–33 years), and…

0301 basic medicineMaleVascular Endothelial Growth Factor AAgingPhysiologySystemic inflammationBiochemistryCarotid Intima-Media Thickness0302 clinical medicineEndocrinologySA-β-Gal activityp21 and p16 genesMedicineTP53Receptor Notch1AortaEndothelial Progenitor CellsAged 80 and overeducation.field_of_studyChemotaxisInflammatory cytokinesmedicine.anatomical_structurecardiovascular systemBiomarker (medicine)Femalemedicine.symptomTP53 p21 and p16 genesSenescenceAdultEndotheliumInflammatory cytokineNotch and TLR4Carotid Artery CommonPopulationProinflammatory cytokine03 medical and health sciencesYoung AdultTP53 p21 and p16 genemedicine.arteryGeneticsHumansEPC cell populationeducationMolecular BiologyEPC cell populationsAgedAortabusiness.industryEndothelium age-related impairmentCell BiologyChemokine CXCL12Toll-Like Receptor 4EPC cell populations; Endothelium age-related impairment; Inflammatory cytokines; Notch and TLR4; SA-β-Gal activity; TP53 p21 and p16 genesSettore MED/23030104 developmental biologyIntima-media thicknessbusiness030217 neurology & neurosurgeryBiomarkersExperimental gerontology
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Uric acid treatment after stroke modulates the Krüppel-like factor 2-VEGF-A axis to protect brain endothelial cell functions: Impact of hypertension

2019

Uric acid (UA) is a promising protective treatment in ischaemic stroke, but the precise molecular targets underlying its in vivo beneficial actions remain unclear. High concentrations of UA inhibit angiogenesis of cultured endothelial cells via Krüppel-like factor 2 (KLF)-induced downregulation of vascular endothelial growth factor (VEGF), a pro-angiogenic mediator that is able to increase blood–brain barrier (BBB) permeability in acute stroke. Here, we investigated whether UA treatment after ischaemic stroke protects brain endothelial cell functions and modulates the KLF2-VEGF-A axis. Transient intraluminal middle cerebral artery (MCA) occlusion/reperfusion was induced in adult male sponta…

0301 basic medicineMaleVascular Endothelial Growth Factor AVascular endothelial growth factor-AAngiogenesisBiochemistryRats Inbred WKYAntioxidantschemistry.chemical_compound0302 clinical medicineRats Inbred SHRIschaemic strokeEvans BlueBlood-brain barrierBrainKrüppel-like factor 2Vascular endothelial growth factorEndothelial stem cellStrokeVascular endothelial growth factor Amedicine.anatomical_structureNeuroprotective AgentsTreatment OutcomeBlood-Brain Barrier030220 oncology & carcinogenesisHypertensioncardiovascular systemmedicine.symptommedicine.medical_specialtyKruppel-Like Transcription FactorsBrain damageBlood–brain barrierNeuroprotectionCell Line03 medical and health sciencesDouble-Blind MethodInternal medicinemedicineAnimalsHumanscardiovascular diseasesPharmacologybusiness.industryRatsUric Acid030104 developmental biologyEndocrinologychemistryEndothelium VascularAngiogenesisbusinessBiomarkers
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Blocking CD248 molecules in perivascular stromal cells of patients with systemic sclerosis strongly inhibits their differentiation toward myofibrobla…

2018

Abstract Background Fibrosis may be considered the hallmark of systemic sclerosis (SSc), the end stage triggered by different pathological events. Transforming growth factor-β (TGF-β) and platelet-derived growth factor BB (PDGF-BB) are profibrotic molecules modulating myofibroblast differentiation and proliferation, respectively. There is evidence linking CD248 with these two molecules, both highly expressed in patients with SSc, and suggesting that CD248 may be a therapeutic target for several diseases. The aim of this work was to evaluate the expression of CD248 in SSc skin and its ability to modulate SSc fibrotic process. Methods After ethical approval was obtained, skin biopsies were co…

0301 basic medicineMalelcsh:Diseases of the musculoskeletal systemProton Pump InhibitorFibrosiCellular differentiationmedicine.medical_treatmentSystemic sclerosiFibrosisImmunology and AllergyMedicineMyofibroblastsskin and connective tissue diseasesCells CulturedSkinintegumentary systemCell DifferentiationMiddle AgedMesenchymal Stem CellBenzamidesSystemic sclerosisFemaleMyofibroblastResearch ArticleHumanAdultStromal cellImmunology03 medical and health sciencesYoung AdultRheumatologyBenzamideAntigens CDAntigens NeoplasmHumansGene silencingCell ProliferationMyofibroblastScleroderma Systemicbusiness.industryGrowth factorMesenchymal stem cellStromal CellMesenchymal Stem CellsProton Pump Inhibitorsmedicine.diseaseFibrosisCD248Settore MED/16 - Reumatologia030104 developmental biologyCancer researchStromal Cellslcsh:RC925-935CD248; Fibrosis; Systemic sclerosis; Rheumatology; Immunology and Allergy; ImmunologybusinessTransforming growth factor
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Effects of resistance training on expression of IGF-I splice variants in younger and older men.

2016

Insulin-like growth factor-I (IGF-I) and its splice variants Insulin-like growth factor-I isoform Ea (IGF-IEa) and mechano growth factor (MGF) may play an important role in muscular adaptations to resistance training (RT) that may be modulated by ageing. It has been suggested that IGF-I induces cellular responses via AKT8 virus oncogene cellular homolog (Akt) and Extracellular signal-regulated kinase (Erk) signalling pathways. Therefore, resistance exercise-induced changes in skeletal muscle IGF-IEa and MGF messenger ribonucleic acid (mRNA), and MGF, Erk1/2, Akt and p70S6K protein expression were investigated before and after 21 weeks of RT in younger (YM, 20–34 yrs., n = 7) and older men (…

0301 basic medicineMalemedicine.medical_specialtyAgingmedicine.medical_treatmentPhysical Therapy Sports Therapy and RehabilitationBiologyMuscle hypertrophy03 medical and health sciences0302 clinical medicineInternal medicineGene expressionmedicinecell signalingHumansProtein IsoformsOrthopedics and Sports Medicinegeeniekspressiomuscle hypertrophyRNA MessengerInsulin-Like Growth Factor Ita315Muscle SkeletalProtein kinase BAgedsoluviestintämechano growth factorOncogeneKinaseGrowth factorSkeletal muscleResistance TrainingGeneral MedicineMiddle Aged030104 developmental biologyEndocrinologymedicine.anatomical_structureikääntyminenageinggene expressionSignal transduction030217 neurology & neurosurgerySignal TransductionEuropean journal of sport science
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Endocrinology of Aging From a Muscle Function Point of View: Results From the Toledo Study for Healthy Aging.

2016

Aging is a process that involves a reduction in muscle strength and anabolic hormone concentrations, which impacts significantly on health.To study the hormone/total strength (H/TS) ratio as a proxy of anabolic insensitivity status in elders, and its relationship with disability, hospitalization, and mortality risk.A total of 1462 persons aged ≥65 years from the Toledo Study of Healthy Aging participated in this study. Serum concentrations of insulin like growth factor 1, total and free testosterone, dehydroepiandrosterone, dehydroepiandrosterone sulfate, and 17β-estradiol were measured. Total maximal voluntary isometric strength was obtained (handgrip, shoulder, hip, and knee) using standa…

0301 basic medicineMalemedicine.medical_specialtyAnabolismmedicine.medical_treatmentDehydroepiandrosteroneEndocrine SystemIsometric exercisePhysical strengthLogistic regressionHealthy Aging03 medical and health scienceschemistry.chemical_compoundInsulin-like growth factor0302 clinical medicineDehydroepiandrosterone sulfateInternal medicinemedicineHumans030212 general & internal medicineMuscle StrengthMuscle SkeletalGeneral NursingAgedbusiness.industryHealth PolicyMortality rateGeneral MedicineHospitalization030104 developmental biologyEndocrinologychemistrySpainFemaleGeriatrics and GerontologybusinessJournal of the American Medical Directors Association
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Anxiolytic effects of muscarinic acetylcholine receptors agonist oxotremorine in chronically stressed rats and related changes in BDNF and FGF2 level…

2017

Rationale: In depressive disorders, one of the mechanisms proposed for antidepressant drugs is the enhancement of synaptic plasticity in the hippocampus and cerebral cortex. Previously, we showed that the muscarinic acetylcholine receptor (mAChR) agonist oxotremorine (Oxo) increases neuronal plasticity in hippocampal neurons via FGFR1 transactivation. Objectives: Here, we aimed to explore (a) whether Oxo exerts anxiolytic effect in the rat model of anxiety-depression-like behavior induced by chronic restraint stress (CRS), and (b) if the anxiolytic effect of Oxo is associated with the modulation of neurotrophic factors, brain-derived neurotrophic factor (BDNF) and fibroblast growth factor-2…

0301 basic medicineMalemedicine.medical_specialtyElevated plus mazemedicine.drug_classBehavioral testPrefrontal CortexHippocampal formationAnxietyMuscarinic AgonistsAnxiolyticHippocampus03 medical and health sciences0302 clinical medicineInternal medicineMuscarinic acetylcholine receptormedicineOxotremorineMuscarinic acetylcholine receptor M4AnimalsElevated plus maze testRats WistarPrefrontal cortexmAChRChronic restraint streForced swimming testPharmacologyNeuronsChemistryBrain-Derived Neurotrophic FactorOxotremorineCerebral cortexRats030104 developmental biologymedicine.anatomical_structureEndocrinologyAnti-Anxiety AgentsCerebral cortexFibroblast Growth Factor 2Anxiety; Behavioral test; Cerebral cortex; Chronic restraint stress; Elevated plus maze test; Forced swimming test; mAChR; Neurotrophins; Novelty suppressed feeding test; PharmacologyNeurotrophinNovelty suppressed feeding testNeuroscience030217 neurology & neurosurgeryStress Psychologicalmedicine.drugPsychopharmacology
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Recombinant human hepatocyte growth factor provides protective effects in cerulein-induced acute pancreatitis in mice.

2018

Acute pancreatitis is a multifactorial disease associated with profound changes of the pancreas induced by release of digestive enzymes that lead to increase in proinflammatory cytokine production, excessive tissue necrosis, edema, and bleeding. Elevated levels of hepatocyte growth factor (HGF) and its receptor c-Met have been observed in different chronic and acute pancreatic diseases including experimental models of acute pancreatitis. In the present study, we investigated the protective effects induced by the recombinant human HGF in a mouse model of cerulein-induced acute pancreatitis. Pancreatitis was induced by 8 hourly administrations of supramaximal cerulein injections (50 µg/kg, ip…

0301 basic medicineMalemedicine.medical_specialtyNecrosisPhysiologyClinical BiochemistryInflammationApoptosismedicine.disease_causeProtective AgentsAntioxidantsProinflammatory cytokine03 medical and health sciencesMiceInternal medicineEdemamedicineAnimalsHumansbusiness.industryHepatocyte Growth FactorCell BiologyProto-Oncogene Proteins c-metmedicine.diseaseGlutathioneSurvival AnalysisRecombinant ProteinsDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyPancreatitisAcute pancreatitisPancreatitisHepatocyte growth factormedicine.symptombusinessOxidative stressCeruletidemedicine.drugSignal TransductionJournal of cellular physiology
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