grant
Molecular mechanisms of progranulin as a regulator of endothelial biology and blood pressure control
Organization UNIVERSITY OF SOUTH ALABAMALocation MOBILE, UNITED STATESPosted 3 Sept 2024Deadline 30 Apr 2029
NIHUS FederalResearch GrantFY2025(hydroxymethylglutaryl-CoA reductase (NADPH)) kinase21+ years old5'-AMP-activated protein kinaseACE InhibitorsAMP-activated kinaseAMP-activated protein kinaseAMPK enzymeAZU1 ProteinActive OxygenAdultAdult HumanAffectAngIIAngiotensin Converting EnzymeAngiotensin I-Converting EnzymeAngiotensin I-Converting Enzyme InhibitorsAngiotensin IIAngiotensin-Converting Enzyme AntagonistsAngiotensin-Converting Enzyme InhibitorsAnti-InflammatoriesAnti-Inflammatory AgentsAnti-inflammatoryAutocrine CommunicationAutocrine SignalingAutocrine SystemsAutomobile DrivingBP controlBP managementBioavailabilityBiological AvailabilityBiologyBlood PressureBlood VesselsCAP 37CAP37CD143 AntigensCarboxycathepsinCardiovascularCardiovascular Body SystemCardiovascular DiseasesCardiovascular Organ SystemCardiovascular systemCell FunctionCell PhysiologyCell ProcessCellular FunctionCellular PhysiologyCellular ProcessCharacteristicsClinicalDataDegenerative Neurologic DisordersDevelopmentDipeptidyl Peptidase ADiseaseDisorderDoseDropsDysfunctionEndogenous Nitrate VasodilatorEndothelial CellsEndotheliumEndothelium-Derived Nitric OxideEnzyme GeneEnzymesExperimental ModelsFunctional disorderGatekeepingGene ModifiedGeneticHBPHMG CoA reductase (NADPH) kinaseHMG CoA reductase kinaseHMG coenzyme A reductase (NADPH) kinaseHeart VascularHeparin Binding ProteinHypertensionIn VitroKO miceKininase AKininase IIKininase II AntagonistsKininase II InhibitorsKnock-out MiceKnockout MiceKnowledgeLengthMediatingMesentericMesenteric ArteriesMesenteryMethodsMiceMice MammalsModelingMolecularMononitrogen MonoxideMurineMusNADPH Oxidase 1Nervous System Degenerative DiseasesNeural Degenerative DiseasesNeural degenerative DisordersNeurodegenerative DiseasesNeurodegenerative DisordersNeurologic Degenerative ConditionsNitric OxideNitrogen MonoxideNitrogen ProtoxideNull MouseOutcomeOxygen RadicalsPC cell-derived growth factorPCDGFPGRN genePGRN proteinPatientsPeptidyl-Dipeptidase APhysiologic AvailabilityPhysiopathologyPredispositionPro-OxidantsProductionProgranulinProteinsPublishingReactive Oxygen SpeciesReceptor ProteinRecombinantsResearchRoleSeriesStimulusSubcellular ProcessSusceptibilityTechnologyTestingTherapeuticUnited StatesVascular DiseasesVascular DisorderVascular Hypertensive DiseaseVascular Hypertensive DisorderVasodilatationVasodilationVasorelaxationWild Type Mouseadulthoodangiotensin hypertensionautocrineblood pressure controlblood pressure managementblood vessel disordercardiovascular disordercationic antimicrobial protein CAP 37circulatory systemdegenerative diseases of motor and sensory neuronsdegenerative neurological diseasesdevelopmentaldrivingendothelial cell derived relaxing factorendothelial dysfunctionexperimentexperimental researchexperimental studyexperimentsgatekeepergene modificationgenetically modifiedgranulin precursorhigh blood pressurehydroxymethylglutaryl-CoA-reductase kinasehyperpiesiahyperpiesishypertension treatmenthypertensivehypertensive diseasehypertensive disorderin vivoinjury to organsinjury to the vasculatureloss of functionmouse modelmurine modelneurodegenerative illnessnew drug targetnew drug treatmentsnew druggable targetnew drugsnew pharmacological therapeuticnew pharmacotherapy targetnew therapeutic targetnew therapeuticsnew therapynew therapy targetnext generation therapeuticsnovelnovel drug targetnovel drug treatmentsnovel druggable targetnovel drugsnovel pharmaco-therapeuticnovel pharmacological therapeuticnovel pharmacotherapy targetnovel therapeutic targetnovel therapeuticsnovel therapynovel therapy targetorgan injuryoverexpressoverexpressionoxidationpathophysiologypharmacologicprogranulin geneprogranulin proteinreceptorsocial roletoolvascularvascular dysfunctionvascular injuryvasculopathywildtype mouse
Description preview
ABSTRACT
Endothelial cell (EC) dysfunction initiates the development of hypertension (HTN), but the mechanisms are not
fully elucidated. Given that HBP is the leading cause of cardiovascular diseases, it is critical to identify new
opportunities to restore EC function in HTN. In a series of supportive preliminary studies, we identified
progranulin…
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