2021
β3 adrenergic receptor as potential therapeutic target in ADPKD
Schena G, Carmosino M, Chiurlia S, Onuchic L, Mastropasqua M, Maiorano E, Schena FP, Caplan MJ. β3 adrenergic receptor as potential therapeutic target in ADPKD. Physiological Reports 2021, 9: e15058. PMID: 34676684, PMCID: PMC8531837, DOI: 10.14814/phy2.15058.Peer-Reviewed Original ResearchConceptsAutosomal dominant polycystic kidney diseaseΒ3-ARΒ3-adrenergic receptorTherapeutic targetKidney/body weight ratioΒ3-AR levelSympathetic nerve activityBody weight ratioType 2 receptorCyst-lining epithelial cellsDominant polycystic kidney diseaseRenal tubular cellsNovel therapeutic targetCyclic AMP accumulationPotential therapeutic targetVasopressin type 2 receptorHuman renal tissuePolycystic kidney diseaseFluid-filled cystsADPKD mouse modelNerve activityKidney functionKidney diseaseRenal parenchymaHealthy controls
2018
Cenicriviroc, a cytokine receptor antagonist, potentiates all‐trans retinoic acid in reducing liver injury in cholestatic rodents
Yu D, Cai S, Mennone A, Vig P, Boyer JL. Cenicriviroc, a cytokine receptor antagonist, potentiates all‐trans retinoic acid in reducing liver injury in cholestatic rodents. Liver International 2018, 38: 1128-1138. PMID: 29356312, PMCID: PMC6032984, DOI: 10.1111/liv.13698.Peer-Reviewed Original ResearchConceptsBile acid pool sizeTrans retinoic acidAcid pool sizePlasma liver enzymesLiver injurySuperior therapeutic effectLiver necrosisLiver enzymesT cellsTherapeutic effectRetinoic acidAntagonist of CCR2Hepatic inflammatory cellsCholestatic liver injuryBile duct proliferationBody weight ratioCholestatic liver diseasePro-inflammatory cytokinesCytokine receptor antagonistsHepatic hydroxyproline contentExpression of cytokinesDuct-ligated ratsBile acid synthesisHepatic infiltrationLiver disease
2017
Rapamycin treatment dose‐dependently improves the cystic kidney in a new ADPKD mouse model via the mTORC1 and cell‐cycle‐associated CDK1/cyclin axis
Li A, Fan S, Xu Y, Meng J, Shen X, Mao J, Zhang L, Zhang X, Moeckel G, Wu D, Wu G, Liang C. Rapamycin treatment dose‐dependently improves the cystic kidney in a new ADPKD mouse model via the mTORC1 and cell‐cycle‐associated CDK1/cyclin axis. Journal Of Cellular And Molecular Medicine 2017, 21: 1619-1635. PMID: 28244683, PMCID: PMC5543471, DOI: 10.1111/jcmm.13091.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibiotics, AntineoplasticCDC2 Protein KinaseCell CycleCyclinsDose-Response Relationship, DrugFemaleFounder EffectGene Expression RegulationHumansIntegrasesKidneyMaleMiceMice, TransgenicMicrofilament ProteinsPolycystic Kidney, Autosomal DominantPromoter Regions, GeneticSignal TransductionSirolimusTOR Serine-Threonine KinasesTRPP Cation ChannelsConceptsAutosomal dominant polycystic kidney diseaseEnd-stage renal diseaseMouse modelCyclin-dependent kinase 1Kidney/body weight ratioPreclinical trialsVivo preclinical resultsBody weight ratioCre transgenic miceHigh-dose rapamycinStandardized animal modelHuman autosomal dominant polycystic kidney diseaseRapamycin (mTOR) inhibitor rapamycinDominant polycystic kidney diseaseMonths of ageOrthologous mouse modelConditional knockout miceDose-dependent mannerPolycystic kidney diseaseAberrant epithelial cell proliferationEpithelial cell proliferationNew molecular targetsADPKD therapyRenal functionADPKD mouse model
2015
Effect of Silodosin, an Alpha1A-Adrenoceptor Antagonist, on Ventral Prostatic Hyperplasia in the Spontaneously Hypertensive Rat
Shimizu S, Shimizu T, Tsounapi P, Higashi Y, Martin DT, Nakamura K, Honda M, Inoue K, Saito M. Effect of Silodosin, an Alpha1A-Adrenoceptor Antagonist, on Ventral Prostatic Hyperplasia in the Spontaneously Hypertensive Rat. PLOS ONE 2015, 10: e0133798. PMID: 26308715, PMCID: PMC4550428, DOI: 10.1371/journal.pone.0133798.Peer-Reviewed Original ResearchMeSH KeywordsActinsAdrenergic alpha-1 Receptor AntagonistsAnimalsChemokine CXCL1Fibroblast Growth Factor 2IndolesInterleukin-6MaleMalondialdehydeProstateProstatic HyperplasiaRatsRats, Inbred SHRReceptors, Adrenergic, alpha-1Regional Blood FlowTransforming Growth Factor beta1Tumor Necrosis Factor-alphaConceptsProstatic blood flowEffects of silodosinBasic fibroblast growth factorAlpha1A-adrenoceptor antagonistInterleukin-6Blood flowBlood pressureProstatic hyperplasiaHypertensive ratsTissue levelsWKY ratsΑ-SMATGF-β1Twelve-week-old male SHRsVentral prostateCytokine-induced neutrophil chemoattractant-1Selective alpha1A-adrenoceptor antagonistAlpha-smooth muscle actinGrowth factor beta 1Neutrophil chemoattractant-1Spontaneously Hypertensive RatsBenign prostatic enlargementBody weight ratioWistar-Kyoto ratsMorphological abnormalitiesProtective effect of hydroxyfasudil, a Rho kinase inhibitor, on ventral prostatic hyperplasia in the spontaneously hypertensive rat
Holmström F, Shimizu S, Shimizu T, Higashi Y, Martin DT, Honda M, Saito M. Protective effect of hydroxyfasudil, a Rho kinase inhibitor, on ventral prostatic hyperplasia in the spontaneously hypertensive rat. The Prostate 2015, 75: 1774-1782. PMID: 26286428, DOI: 10.1002/pros.23063.Peer-Reviewed Original ResearchConceptsVentral prostateBlood pressureHypertensive ratsWKY ratsInflammatory cytokinesProstatic hyperplasiaIL-6Growth factorΑ-SMATGF-β1Twelve-week-old SHRMorphological abnormalitiesROCK activityTail-cuff methodBody weight ratioWistar-Kyoto ratsHypertensive rat modelSmooth muscle contractionRho-kinase pathwayWeeks of ageRho-kinase inhibitorSmooth muscle differentiation markersInflammatory markersChronic treatmentProstate weight
2014
Pathological Changes in Pulmonary Circulation in Carbon Tetrachloride (ccl4)-Induced Cirrhotic Mice
Das M, Boerma M, Goree JR, Lavoie EG, Fausther M, Gubrij IB, Pangle AK, Johnson LG, Dranoff JA. Pathological Changes in Pulmonary Circulation in Carbon Tetrachloride (ccl4)-Induced Cirrhotic Mice. PLOS ONE 2014, 9: e96043. PMID: 24763616, PMCID: PMC3999097, DOI: 10.1371/journal.pone.0096043.Peer-Reviewed Original ResearchConceptsPulmonary acceleration timeCirrhotic micePortopulmonary hypertensionPulmonary circulationPathological changesSpleen weight/body weight ratioVentricle weight/body weightWeight/body weight ratioChronic CCl4 treatmentPulmonary vascular diseaseMale C57BL/6 miceBody weight ratioTimes/weekOxidative stress markersNovel therapeutic interventionsPicrosirius red stainingSterile olive oilPortal hypertensionEffects of CCl4Pulmonary arteryC57BL/6 micePathophysiological mechanismsPulmonary vasculaturePerivascular collagenVascular disease
2013
Effect of patient Age on surgical outcomes for Graves’ disease: a case–control study of 100 consecutive patients at a high volume thyroid surgical center
Breuer CK, Solomon D, Donovan P, Rivkees SA, Udelsman R. Effect of patient Age on surgical outcomes for Graves’ disease: a case–control study of 100 consecutive patients at a high volume thyroid surgical center. International Journal Of Pediatric Endocrinology 2013, 2013: 1. PMID: 23351530, PMCID: PMC3574836, DOI: 10.1186/1687-9856-2013-1.Peer-Reviewed Original ResearchPermanent hypoparathyroidismTotal thyroidectomyConsecutive patientsPatient ageOperative timeSurgery teamTransient recurrent laryngeal nerve dysfunctionRecurrent laryngeal nerve injuryRecurrent laryngeal nerve dysfunctionLaryngeal nerve injuryPost-operative hypocalcemiaSummary of backgroundLonger operative timeBody weight ratioLength of stayCase-control studyConclusionSurgical managementPediatric thyroidTemporary hypocalcemiaNerve dysfunctionOperative mortalityNeck hematomaNerve injuryPostoperative hematomaComplication rate
2010
Deletion of Irs2 causes reduced kidney size in mice: role for inhibition of GSK3β?
Carew R, Sadagurski M, Goldschmeding R, Martin F, White M, Brazil D. Deletion of Irs2 causes reduced kidney size in mice: role for inhibition of GSK3β? BMC Developmental Biology 2010, 10: 73. PMID: 20604929, PMCID: PMC2910663, DOI: 10.1186/1471-213x-10-73.Peer-Reviewed Original ResearchConceptsIrs2-/- miceYes-Associated ProteinKidney sizeΒ-cateninΒ-catenin targetsBody weight ratioImportant novel mediatorType 2 diabetesPostnatal day 5Mouse developmentInhibition of GSK3βOrgan sizeYAP activityYAP phosphorylationPituitary developmentDevelopmental defectsYAP levelsGlomerular densityRenal growthNeuronal proliferationAnalysis of insulinGlomerular numberConcomitant accumulationDay 5Kidney structureTelmisartan regresses left ventricular hypertrophy in caveolin-1-deficient mice
Kreiger M, Di Lorenzo A, Teutsch C, Kauser K, Sessa WC. Telmisartan regresses left ventricular hypertrophy in caveolin-1-deficient mice. Laboratory Investigation 2010, 90: 1573-1581. PMID: 20585312, PMCID: PMC3248785, DOI: 10.1038/labinvest.2010.116.Peer-Reviewed Original ResearchConceptsCav-1 KO miceAngiotensin receptor blockersKO miceCardiac functionLV hypertrophyWT miceCardiac hypertrophyΒ-myosin heavy chainBody weight ratioTibial length ratioNatriuretic peptide ACaveolin-1-deficient miceCav-1 KOReceptor blockersPerivascular fibrosisVentricular hypertrophyVentricular weightAngiotensin IIIntramyocardial vesselsSpontaneous modelUnique genetic modelHypertrophyMiceTreatmentCaveolin-1Alterations of pre- and postsynaptic noradrenergic signaling in a rat model of adriamycin-induced cardiotoxicity
Kenk M, Thackeray JT, Thorn SL, Dhami K, Chow BJ, Ascah KJ, DaSilva JN, Beanlands RS. Alterations of pre- and postsynaptic noradrenergic signaling in a rat model of adriamycin-induced cardiotoxicity. Journal Of Nuclear Cardiology 2010, 17: 254-263. PMID: 20182926, DOI: 10.1007/s12350-009-9190-x.Peer-Reviewed Original ResearchConceptsPositron emission tomographyRat modelNoradrenergic signalingHeart/body weight ratioBeta-adrenergic receptor antagonistMyocardial noradrenaline levelsSympathetic nervous systemBody weight ratioPhosphodiesterase 4 inhibitorBeta-adrenergic receptorsVentricle free wallAnthracycline chemotherapeutic agentDesipramine treatmentNoradrenaline levelsNoradrenaline uptakeAnthracycline cardiotoxicityReceptor antagonistAcute increaseCardiac functionRight ventricleLeft atriumInteraction of preAdriamycin cardiotoxicityFree wallNervous system
2009
ERK1/2-Dependent Vascular Endothelial Growth Factor Signaling Sustains Cyst Growth in Polycystin-2 Defective Mice
Spirli C, Okolicsanyi S, Fiorotto R, Fabris L, Cadamuro M, Lecchi S, Tian X, Somlo S, Strazzabosco M. ERK1/2-Dependent Vascular Endothelial Growth Factor Signaling Sustains Cyst Growth in Polycystin-2 Defective Mice. Gastroenterology 2009, 138: 360-371.e7. PMID: 19766642, PMCID: PMC3000794, DOI: 10.1053/j.gastro.2009.09.005.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedCyclic AMP-Dependent Protein KinasesCystsHypoxia-Inducible Factor 1, alpha SubunitIndolesLiver DiseasesMAP Kinase Signaling SystemMiceMice, KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhenotypePhosphorylationProliferating Cell Nuclear AntigenProtein Kinase InhibitorsPyrrolesRepressor ProteinsTRPP Cation ChannelsTumor Suppressor ProteinsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ConceptsVascular endothelial growth factorPolycystic liver diseaseVEGF secretionLiver cystsLiver diseaseVEGFR-2Cyst growthLiver/body weight ratioAdult dominant polycystic kidney diseaseParacrine vascular endothelial growth factorSecretion of VEGFHIF-1alphaBody weight ratioEffects of VEGFAutocrine vascular endothelial growth factorDominant polycystic kidney diseaseExpression of pERKVascular endothelial growth factor signalingPhosphorylated VEGFR-2Liver cyst growthEndothelial growth factorPolycystic kidney diseaseCyst epithelial cellsExtracellular signal-regulated kinase 1/2Hypoxia-inducible factor
2005
Protection from angiotensin II‐induced cardiac hypertrophy and fibrosis by systemic lentiviral delivery of ACE2 in rats
Huentelman MJ, Grobe JL, Vazquez J, Stewart JM, Mecca AP, Katovich MJ, Ferrario CM, Raizada MK. Protection from angiotensin II‐induced cardiac hypertrophy and fibrosis by systemic lentiviral delivery of ACE2 in rats. Quarterly Journal Of Experimental Physiology And Cognate Medical Sciences 2005, 90: 783-790. PMID: 16049057, DOI: 10.1113/expphysiol.2005.031096.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin IIAngiotensin-Converting Enzyme 2AnimalsAnimals, NewbornBlood PressureBody WeightCarboxypeptidasesCardiomyopathy, HypertrophicEndomyocardial FibrosisGene ExpressionGenetic VectorsHeartLentivirusMiceMyocardiumOrgan SizePeptidyl-Dipeptidase ARatsRats, Sprague-DawleyTransduction, GeneticConceptsRenin-angiotensin systemAngiotensin IIMyocardial fibrosisCardiac hypertrophyAngiotensin II infusionSystolic blood pressureBody weight ratioOverexpression of ACE2Potential therapeutic targetII infusionMmHg increaseBlood pressureHeart weightControl ratsDawley ratsCardiovascular diseaseEnzyme 2Protective effectTherapeutic targetMouse ACE2FibrosisHypertrophyRatsACE2Significant attenuation
2004
Pharmacological Inhibition and Genetic Deficiency of Plasminogen Activator Inhibitor-1 Attenuates Angiotensin II/Salt-Induced Aortic Remodeling
Weisberg AD, Albornoz F, Griffin JP, Crandall DL, Elokdah H, Fogo AB, Vaughan DE, Brown NJ. Pharmacological Inhibition and Genetic Deficiency of Plasminogen Activator Inhibitor-1 Attenuates Angiotensin II/Salt-Induced Aortic Remodeling. Arteriosclerosis Thrombosis And Vascular Biology 2004, 25: 365-371. PMID: 15576638, DOI: 10.1161/01.atv.0000152356.85791.52.Peer-Reviewed Original ResearchMeSH KeywordsAcetatesAdministration, OralAngiotensin IIAnimalsAntigens, DifferentiationAortaAortic DiseasesBlood PressureChemokine CCL2Collagen Type ICollagen Type IIIDrug Evaluation, PreclinicalFibronectinsFibrosisGene Expression RegulationGlomerulosclerosis, Focal SegmentalHeartHypertrophy, Left VentricularIndoleacetic AcidsIndolesKidneyMaleMiceMice, Inbred C57BLMice, KnockoutMyocardiumNephrectomyOsteopontinPlasminogen Activator Inhibitor 1Random AllocationRNA, MessengerSialoglycoproteinsSingle-Blind MethodSodium Chloride, DietaryConceptsAng IIAortic remodelingCardiac fibrosisPAI-039PAI-1 inhibitionVascular remodelingCardiac hypertrophyMouse modelHeart/body weight ratioAng II/saltWall thickeningPharmacological inhibitionSmall molecule PAI-1 inhibitorAortic mRNA expressionHigh salt intakeAortic wall thickeningMale C57BL/6J miceBody weight ratioChemoattractant protein-1PAI-1 deficiencyPAI-1 activityPAI-1 inhibitorPlasminogen activator inhibitorPressor responseAngiotensin II
2000
G1 kinases and transforming growth factor-β; signaling are associated with a growth pattern switch in diabetes-induced renal growth
Huang H, Preisig P. G1 kinases and transforming growth factor-β; signaling are associated with a growth pattern switch in diabetes-induced renal growth. Kidney International 2000, 58: 162-172. PMID: 10886561, DOI: 10.1046/j.1523-1755.2000.00151.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCDC2-CDC28 KinasesCyclin ECyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent KinasesDiabetes Mellitus, ExperimentalDiabetic NephropathiesDNA-Binding ProteinsG1 PhaseHyperplasiaHypertrophyKidney Tubules, ProximalMaleProtein Serine-Threonine KinasesProto-Oncogene ProteinsRatsRats, Sprague-DawleyReceptors, Transforming Growth Factor betaSignal TransductionSmad2 ProteinSmad4 ProteinTrans-ActivatorsTransforming Growth Factor betaConceptsReceptor II expressionCyclin E kinase activityReceptor expressionRenal growthGrowth factor beta receptor expressionTGF-beta receptor II expressionBaseline levelsProximal tubule cell growthTGF-beta receptor expressionBody weight ratioCdk2/cyclin E kinase activityCdk2/cyclin E complexesCyclin DRenal proximal tubulesDiabetes mellitusDiabetic ratsTGF-beta signalingDiabetic stateCyclin E complexGrowth patternDay 2Proximal tubulesDay 4Day 10Tubule growth
1990
Enhanced Susceptibility to Histamine-Induced Cardiac Arrhythmias in Spontaneously Hypertensive Rats
Cameron J, Swigart C, Shin G, Katz D, Bassett A. Enhanced Susceptibility to Histamine-Induced Cardiac Arrhythmias in Spontaneously Hypertensive Rats. Journal Of Cardiovascular Pharmacology 1990, 15: 626-632. PMID: 1691394, DOI: 10.1097/00005344-199004000-00016.Peer-Reviewed Original ResearchConceptsIncidence of arrhythmiasSpontaneous firing rateAction potential durationHypertensive ratsH2-receptor blocker cimetidineFiring rateElevated intracellular calcium levelsSpontaneously Hypertensive RatsBody weight ratioLevels of repolarizationCardiac rhythm disturbancesChannel antagonist verapamilAge-matched controlsIntracellular calcium levelsEnhanced susceptibilitySHR ventriclesWKY preparationsSHR heartsAntagonist verapamilArrhythmogenic influenceRhythm disturbancesHistamine releaseMyocardial hypertrophySHR myocardiumDrug levels
1989
Histamine attenuates the arrhythmogenic effects of norepinephrine in hearts of spontaneously hypertensive rats
Cameron J, Katz D, Swigart C, Bassett A. Histamine attenuates the arrhythmogenic effects of norepinephrine in hearts of spontaneously hypertensive rats. European Journal Of Pharmacology 1989, 169: 23-31. PMID: 2532144, DOI: 10.1016/0014-2999(89)90813-3.Peer-Reviewed Original ResearchConceptsHypertensive ratsArrhythmogenic effectsH2-receptor antagonist cimetidineSetting of hypertensionBody weight ratioLevels of repolarizationSpontaneous firing rateNorepinephrine-induced increaseSex-matched controlsAction potential durationCardiac histamineSHR ventriclesWKY preparationsAdrenoceptor functionHypertensive heartAntagonist cimetidineRhythm disturbancesMyocardial hypertrophyPotential durationDrug AdministrationLeft ventriclePercent incidenceNorepinephrineFiring rateHistamine
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