2005
Regression of Existing Glomerulosclerosis by Inhibition of Aldosterone
Aldigier JC, Kanjanbuch T, Ma LJ, Brown NJ, Fogo AB. Regression of Existing Glomerulosclerosis by Inhibition of Aldosterone. Journal Of The American Society Of Nephrology 2005, 16: 3306-3314. PMID: 16192423, DOI: 10.1681/asn.2004090804.Peer-Reviewed Original ResearchConceptsInhibition of aldosteroneAngiotensin type 1 receptor antagonistType 1 receptor antagonistAdult male Sprague-DawleySeverity of glomerulosclerosisDevelopment of glomerulosclerosisMale Sprague-DawleyEffect of inhibitionCONT ratsGlomerulosclerosis indexSerum creatinineSystolic BPAntihypertensive drugsReceptor antagonistSprague-DawleySP ratsGlomerulosclerosisSpironolactoneSame ratsRatsSP groupAldosteroneFurther treatmentWkInhibition
2003
Tissue- and agonist-specific regulation of human and murine plasminogen activator inhibitor-1 promoters in transgenic mice
Eren M, Painter CA, Gleaves LA, Schoenhard JA, Atkinson JB, Brown NJ, Vaughan DE. Tissue- and agonist-specific regulation of human and murine plasminogen activator inhibitor-1 promoters in transgenic mice. Journal Of Thrombosis And Haemostasis 2003, 1: 2389-2396. PMID: 14629474, DOI: 10.1046/j.1538-7836.2003.00437.x.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin IIAnimalsGene Expression RegulationGreen Fluorescent ProteinsHumansImmunohistochemistryLipopolysaccharidesLuminescent ProteinsMiceMice, TransgenicOrgan SpecificityPlasminogen Activator Inhibitor 1Promoter Regions, GeneticTissue DistributionTransforming Growth Factor betaTransforming Growth Factor beta1ConceptsTranscriptional responseMurine PAI-1Plasminogen activator inhibitor-1 promoterPhysiological regulationPAI-1 promoterPlasminogen activator inhibitor type 1 (PAI-1) expressionGreen fluorescent proteinAgonist-specific regulationTranscription factorsTransgenic strategiesTransgenic miceDNA sequencesPAI-1 expressionHeterologous promoterAng IIQuantitative regulationRegulatory mechanismsRegulatory factorsFluorescent proteinKb promoterTransgenic animalsPhysiological relevancePromoterFunctional studiesEGFP expression
2002
Potential Roles of Plasminogen Activator System in Coronary Vascular Remodeling Induced by Long-term Nitric Oxide Synthase Inhibition
Kaikita K, Schoenhard JA, Painter CA, Ripley RT, Brown NJ, Fogo AB, Vaughan DE. Potential Roles of Plasminogen Activator System in Coronary Vascular Remodeling Induced by Long-term Nitric Oxide Synthase Inhibition. Journal Of Molecular And Cellular Cardiology 2002, 34: 617-627. PMID: 12054849, DOI: 10.1006/jmcc.2002.2001.Peer-Reviewed Original ResearchConceptsSystolic blood pressureNitric oxide synthase inhibitionOxide synthase inhibitionPerivascular fibrosisBlood pressurePAI-1 deficiencyCoronary perivascular fibrosisPlasminogen activator systemL-NAMENOS inhibitionSynthase inhibitionDeficient miceVascular pathologyLong-term nitric oxide synthase inhibitionNitro-L-arginine methyl esterL-NAME-induced hypertensionLong-term NOS inhibitionPlasma TGF-beta1 levelsPlasminogen activator inhibitor-1-deficient miceStructural vascular changesTGF-beta1 levelsLong-term treatmentTissue-type plasminogen activator-deficient miceWeek study periodActivator system