Search results for "Vascular system"

showing 10 items of 4322 documents

Molecular chaperones in the brain endothelial barrier: neurotoxicity or neuroprotection?

2019

Brain microvascular endothelial cells (BMECs) interact with astrocytes and pericytes to form the blood-brain barrier (BBB). Their compromised function alters the BBB integrity, which is associated with early events in the pathogenesis of cancer, neurodegenerative diseases, and epilepsy. Interestingly, these conditions also induce the expression of heat shock proteins (HSPs). Here we review the contribution of major HSP families to BMEC and BBB function. Although investigators mainly report protective effects of HSPs in brain, contrasted results were obtained in BMEC, which depend both on the HSP and on its location, intra- or extracellular. The therapeutic potential of HSPs must be scrupulo…

0301 basic medicineReviewBiochemistryNeuroprotectionPathogenesis03 medical and health sciencesEpilepsy0302 clinical medicineHeat shock proteinGeneticsExtracellularMedicineAnimalsHumansMolecular Biologybusiness.industryNeurotoxicityCancerBrainEndothelial CellsBiological TransportCell Differentiationmedicine.diseaseNeuroprotectionCell biology030104 developmental biologyBlood-Brain Barriercardiovascular systembusiness030217 neurology & neurosurgeryFunction (biology)BiotechnologyMolecular ChaperonesFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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The angiotensin‐(1‐7)/Mas receptor axis protects from endothelial cell senescence via klotho and Nrf2 activation

2019

Endothelial cell senescence is a hallmark of vascular aging that predisposes to vascular disease. We aimed to explore the capacity of the renin-angiotensin system (RAS) heptapeptide angiotensin (Ang)-(1-7) to counteract human endothelial cell senescence and to identify intracellular pathways mediating its potential protective action. In human umbilical vein endothelial cell (HUVEC) cultures, Ang II promoted cell senescence, as revealed by the enhancement in senescence-associated galactosidase (SA-β-gal+) positive staining, total and telomeric DNA damage, adhesion molecule expression, and human mononuclear adhesion to HUVEC monolayers. By activating the G protein-coupled receptor Mas, Ang-(1…

0301 basic medicineSenescenceAgingNF-E2-Related Factor 2medicine.medical_treatmentCellBiologyKlothoReceptors G-Protein-Coupled03 medical and health sciences0302 clinical medicineheme oxygenase‐1medicineHuman Umbilical Vein Endothelial CellsHumansReceptorKlothoKlotho ProteinsCells CulturedCellular SenescenceGlucuronidaseangiotensin‐(1‐7)Original PaperNuclear factor (erythroid-derived 2)-like 2nuclear factor (erythroid‐derived 2)‐like 2Vascular agingCell BiologyAngiotensin-(1-7)FarmaciaOriginal PapersPeptide FragmentsEndothelial senescenceCell biologyEndothelial stem cell030104 developmental biologyCytokinemedicine.anatomical_structureHeme oxygenase-1cardiovascular systemHuman umbilical vein endothelial cellAngiotensin I030217 neurology & neurosurgeryIntracellular
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Mediterranean nutraceutical foods: Strategy to improve vascular ageing.

2015

Ageing is characterized by a decline in all systemic functions. A greater susceptibility to apoptosis and senescence may contribute to proliferative and functional impairment of endothelial progenitor cells. They play an important role in neo-angiogenesis and endothelial repair. Vascular ageing is associated with changes in the structure and functions of vessels' wall. There are many possible causes of this damage. For sure, inflammation and oxidative stress play a fundamental role in the pathogenesis of endothelial dysfunction, commonly attributed to a reduced availability of nitric oxide. Inflammageing, the chronic low-grade inflammation that characterizes elderly people, aggravates vascu…

0301 basic medicineSenescencePathologymedicine.medical_specialtyAgingInflammationDisease030204 cardiovascular system & hematologyBioinformaticsmedicine.disease_causeDiet MediterraneanEndothelial progenitor cellPathogenesis03 medical and health sciences0302 clinical medicineNutraceuticalmedicineHumansVascular DiseasesEndothelial dysfunctionEndothelial Progenitor CellsSettore MED/04 - Patologia Generalebusiness.industryVascular ageingmedicine.diseaseInflammageing030104 developmental biologyAgeingNutraceuticalEndothelium Vascularmedicine.symptombusinessOxidative stressDevelopmental BiologyMechanisms of ageing and development
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Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways

2020

Background: Early nutrition influences the risk of Chronic Kidney Diseases development in adulthood. Mechanisms underlying the early programming of altered renal function remain incompletely understood. This study aims at characterizing the role of cell senescence pathways in early programming of Chronic Kidney Disease after transient postnatal overfeeding. Material and Methods: Reduced litters of 3 mice pups and standard litters of 10 mice pups were obtained to induce overfed animals during lactation and control animals, respectively. Animals were sacrificed at 24 days (weaning) or at 7 months of life (adulthood). Body weight, blood pressure, kidney weight, and glomerular count were assess…

0301 basic medicineSenescencekidneymedicine.medical_specialtyPhysiologyRenal function030204 cardiovascular system & hematologyprogramming[SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrologylcsh:Physiology03 medical and health sciencesovernutrition0302 clinical medicineOvernutritionPhysiology (medical)Internal medicineLactationmedicineWeaningOriginal Research2. Zero hungerKidneypostnatal overfeedinglcsh:QP1-981biologySirtuin 1medicine.disease[SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and Nephrologychronic kidney disease; developmental origins of health and disease; kidney; overnutrition; postnatal overfeeding; programming[SDV.AEN] Life Sciences [q-bio]/Food and Nutrition030104 developmental biologymedicine.anatomical_structureEndocrinologybiology.proteindevelopmental origins of health and disease[SDV.AEN]Life Sciences [q-bio]/Food and Nutritionchronic kidney diseaseKidney diseaseFrontiers in Physiology
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Anti-PCSK9 treatment: is ultra-low low-density lipoprotein cholesterol always good?

2018

Anti-PCSK9 (proprotein convertase subtilisin kexin 9) monoclonal antibodies (Mab) are novel, potent lipid-lowering drugs. They demonstrated to improve the lipid profile in high cardiovascular risk patients. Anti-PCSK9 Mab inhibit the targeted low-density lipoprotein (LDL)-receptor degradation induced by PCSK9 protein and are able to reduce LDL cholesterol (LDL-C) levels on top of conventional lipid-lowering therapy. Though these drugs proved to be very safe in the short-term, little is known about the possible long-term effects, due to the short period of their marketing. The genetic low cholesterol syndromes (LCS) represent the natural models of the lipid-lowering anti-PCSK9 therapy, and a…

0301 basic medicineSerine Proteinase InhibitorsTime FactorsPhysiologymedicine.drug_class030204 cardiovascular system & hematologyPharmacologyMonoclonal antibodyRisk Assessment03 medical and health sciencesPCSK9 Genechemistry.chemical_compound0302 clinical medicineRisk FactorsPhysiology (medical)Diabetes mellitusmedicineAnimalsHumansDyslipidemiasmedicine.diagnostic_testbusiness.industryCholesterolPCSK9Anticholesteremic AgentsPCSK9 InhibitorsAntibodies MonoclonalCholesterol LDLmedicine.diseaseFatty LiverHypocholesterolemia030104 developmental biologyTreatment OutcomechemistryDiabetes Mellitus Type 2lipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineLipid profilebusinessCognition DisordersBiomarkersLipoproteinCardiovascular research
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Coronary Serum Obtained After Myocardial Infarction Induces Angiogenesis and Microvascular Obstruction Repair. Role of Hypoxia-inducible Factor-1A.

2017

Microvascular obstruction (MVO) exerts deleterious effects following acute myocardial infarction (AMI). We investigated coronary angiogenesis induced by coronary serum and the role of hypoxia-inducible factor-1A (HIF-1A) in MVO repair.Myocardial infarction was induced in swine by transitory 90-minute coronary occlusion. The pigs were divided into a control group and 4 AMI groups: no reperfusion, 1minute, 1 week and 1 month after reperfusion. Microvascular obstruction and microvessel density were quantified. The proangiogenic effect of coronary serum drawn from coronary sinus on endothelial cells was evaluated using an in vitro tubulogenesis assay. Circulating and myocardial HIF-1A levels an…

0301 basic medicineSerummedicine.medical_specialtyAngiogenesisSwineSus scrofaMyocardial InfarctionNeovascularization Physiologic030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicineInternal medicinemedicineAnimalscardiovascular diseasesMyocardial infarctionLigationbusiness.industryEndothelial CellsGeneral Medicinemedicine.diseaseHypoxia-Inducible Factor 1 alpha Subunit030104 developmental biologyHypoxia-inducible factorsCoronary OcclusionMicrovesselsCardiologyFemalebusinesshuman activitiesRevista espanola de cardiologia (English ed.)
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Characterization of a mutant form of human apolipoprotein B (Thr26_Tyr27del) associated with familial hypobetalipoproteinemia

2016

We have previously identified a deletion mutant of human apoB [apoB (Thr26_Tyr27del)] in a subject with primary hypobetalipoproteinemia. The present study determined the effect of Thr26_Tyr27del mutation on apoB secretion using transfected McA-RH7777 cells. Transient or stable transfection of apoB-48 containing the Thr26_Tyr27del mutation showed drastically reduced secretion of the mutant as compared to wild-type apoB-48. No lipoproteins containing the mutant apoB-48 were secreted into the medium. Incubation of transfected cells in a lipid-rich medium in the presence of cycloheximide showed rapid turnover of cell-associated mutant apoB-48 as compared to that of wild-type apoB-48. Immunofluo…

0301 basic medicineSettore MED/09 - Medicina InternaTime FactorsApolipoprotein B-48 secretionApolipoprotein BMutantDNA Mutational AnalysisApolipoprotein B mutation Apolipoprotein B-48 secretion Hypobetalipoproteinemia Proteasomal degradation030204 cardiovascular system & hematologymedicine.disease_causeEndoplasmic ReticulumHypobetalipoproteinemiaschemistry.chemical_compound0302 clinical medicineProteasomal degradationProteolysiSequence DeletionMutationbiologyMedicine (all)TransfectionProteasome InhibitorPhenotypeBiochemistryApolipoprotein B-100lipids (amino acids peptides and proteins)Proteasome InhibitorsHumanHeterozygoteProteasome Endopeptidase ComplexTime FactorCycloheximideTransfectiondigestive systemCell LineDNA Mutational Analysi03 medical and health sciencesmedicineHumansSecretionGenetic Predisposition to DiseaseMolecular BiologyEndoplasmic reticulumnutritional and metabolic diseasesCell Biologymedicine.diseaseMolecular biology030104 developmental biologychemistryProteolysisbiology.proteinHypobetalipoproteinemiaApolipoprotein B mutationApolipoprotein B-48Hypobetalipoproteinemia
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Altilix® Supplement Containing Chlorogenic Acid and Luteolin Improved Hepatic and Cardiometabolic Parameters in Subjects with Metabolic Syndrome: A 6…

2019

The objective was to evaluate the effects of 6 months of supplementation with Altilix&reg

0301 basic medicineSettore MED/09 - Medicina Internacynaragenetic structuresPlacebo-controlled study030204 cardiovascular system & hematologySettore BIO/09 - FisiologiaGastroenterology0302 clinical medicineDiabetes mellitusimmune system diseasescardiovascular diseasehemic and lymphatic diseasesBrachial arteryLuteolinNutrition and Dieteticsdiabetes mellituFatty liverhemic and immune systemsDietary supplementsMetabolic syndromeCardiovascular diseasesLivertype 2diabetes mellitusChlorogenic Acidlcsh:Nutrition. Foods and food supplymedicine.medical_specialtyWaistlcsh:TX341-641chemical and pharmacologic phenomenaCynaraPlacebometabolic syndromedietary supplements03 medical and health sciencesDouble-Blind MethodInternal medicineDiabetes mellitusmedicine.arterymedicinebusiness.industrynon-alcoholic fatty liver diseasemedicine.diseasecardiovascular diseases030104 developmental biologydietary supplementSteatosisMetabolic syndromebusinessFood ScienceNon-alcoholic fatty liver disease
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PCSK9-D374Y mediated LDL-R degradation can be functionally inhibited by EGF-A and truncated EGF-A peptides: An in vitro study.

2019

Abstract Background and aims Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to low density lipoprotein receptor (LDLR) through the LDLR epidermal growth factor-like repeat A (EGF-A) domain and induces receptor internalization and degradation. PCSK9 has emerged as a novel therapeutic target for hypercholesterolemia. Clinical studies with PCSK9 inhibiting antibodies have demonstrated strong LDL-c lowering effects, but other therapeutic approaches using small molecule inhibitors for targeting PCSK9 functions may offer supplementary therapeutic options. The aim of our study was to evaluate the effect of synthetic EGF-A analogs on mutated (D374Y) PCSK9-D374Y mediated LDLR degradatio…

0301 basic medicineSmall peptidesmedia_common.quotation_subject030204 cardiovascular system & hematologyDecoy strategyPCSK903 medical and health sciences0302 clinical medicineHumansInternalizationCells Culturedmedia_commonExpression vectorEpidermal Growth FactorChemistryPCSK9PCSK9 InhibitorsTransfectionProprotein convertasePCSK9 inhibitionIn vitroCell biologyEGF-A domain030104 developmental biologyLDLRReceptors LDLLDL receptorMutationKexinlipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
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Collapsibility of the internal jugular veins in the lateral decubitus body position: A potential protective role of the cerebral venous outflow again…

2019

Recent research has revealed that patients with neurodegenerative disease sleep longer in the supine position, while healthy controls prefer sleeping in the lateral decubitus position. Thus, sleeping in the lateral position seems to be protective against neurodegeneration. It has also been suggested that a protective role of this body position could be associated with better cerebral venous drainage in this body position, which results in more active glymphatic system of the brain (the system responsible for clearance of the cerebral tissue from waste products, e.g. amyloid-β). Since no published evidence exists regarding venous outflow from the cranial cavity in the lateral decubitus posit…

0301 basic medicineSupine positionModels NeurologicalPostureBlood PressurePilot ProjectsLateral decubitus positionSitting03 medical and health sciencesHabits0302 clinical medicineAlzheimer DiseaseReference Valuesmental disordersCranial cavitymedicineLateral Decubitus PositionSupine PositionHumansNeurodegenerationInternal jugular veinhealth care economics and organizationsUltrasonographyRight Lateral Decubitus PositionAquaporin 4business.industryNeurodegenerationHemodynamicsGeneral MedicineAnatomyAlzheimer's diseasemedicine.diseaseCerebral Veins030104 developmental biologymedicine.anatomical_structureCerebrovascular CirculationPulsatile FlowNerve Degenerationcardiovascular systemInternal jugular veinGlymphatic systemJugular VeinsbusinessSleepGlymphatic System030217 neurology & neurosurgeryBlood Flow VelocityMedical hypotheses
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