2023
Endothelial Dysfunction in Cardiorenal Conditions: Implications of Endothelial Glucocorticoid Receptor-Wnt Signaling
Akhter M, Goodwin J. Endothelial Dysfunction in Cardiorenal Conditions: Implications of Endothelial Glucocorticoid Receptor-Wnt Signaling. International Journal Of Molecular Sciences 2023, 24: 14261. PMID: 37762564, PMCID: PMC10531724, DOI: 10.3390/ijms241814261.Peer-Reviewed Original ResearchConceptsGlucocorticoid receptorEndothelial dysfunctionVascular inflammationEndothelial cellsEndothelial glucocorticoid receptorAnti-inflammatory effectsFatty acid oxidation pathwayDifferent pathological conditionsSuppression of WntRenal diseaseInflammatory cascadeVascular toneNovel therapiesMultiple organsBlood fluidityEndothelial integrityPlatelet aggregationInnermost liningVessel permeabilityBlood vesselsPathological conditionsWnt pathwayInflammationDysfunctionDevastating disease
2021
Interactions among Long Non-Coding RNAs and microRNAs Influence Disease Phenotype in Diabetes and Diabetic Kidney Disease
Srivastava SP, Goodwin JE, Tripathi P, Kanasaki K, Koya D. Interactions among Long Non-Coding RNAs and microRNAs Influence Disease Phenotype in Diabetes and Diabetic Kidney Disease. International Journal Of Molecular Sciences 2021, 22: 6027. PMID: 34199672, PMCID: PMC8199750, DOI: 10.3390/ijms22116027.Peer-Reviewed Original ResearchConceptsDiabetic kidney diseaseKidney diseaseLarge-scale RNA sequencingGenome-wide profiling dataLong non-coding RNAsNon-coding RNAsDisease phenotypeTherapeutic targetNoncoding RNAsRNA sequencingPathogenesis of diabetesPotential therapeutic targetCrosstalk mechanismsRegulatory microRNAsCrosstalk interactionsLncRNAsMechanism of actionProfiling dataMicroRNAsAberrant expressionDiverse targetsDisease processDiabetesRNADiseaseLoss of endothelial glucocorticoid receptor accelerates diabetic nephropathy
Srivastava SP, Zhou H, Setia O, Liu B, Kanasaki K, Koya D, Dardik A, Fernandez-Hernando C, Goodwin J. Loss of endothelial glucocorticoid receptor accelerates diabetic nephropathy. Nature Communications 2021, 12: 2368. PMID: 33888696, PMCID: PMC8062600, DOI: 10.1038/s41467-021-22617-y.Peer-Reviewed Original ResearchMeSH KeywordsAdrenalectomyAnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesEndothelial CellsEndotheliumEpithelial-Mesenchymal TransitionFatty AcidsFibrosisGlucocorticoidsHumansHypercholesterolemiaInterleukin-6Kidney TubulesMaleMiceMice, Knockout, ApoEOxidation-ReductionReceptors, GlucocorticoidStreptozocinWnt Signaling PathwayConceptsEndothelial glucocorticoid receptorGlucocorticoid receptorEndothelial cell homeostasisDiabetic miceRenal fibrosisEndothelial cellsMesenchymal transitionSevere renal fibrosisTubular epithelial cellsCell homeostasisFatty acid oxidationDiabetic controlDiabetic nephropathyAntifibrotic moleculesIL-6Kidney fibrosisMesenchymal activationRegulation of diseaseOrgan fibrosisAberrant cytokineFibrogenic phenotypeFibrosisMiceEpithelial cellsDefective regulation
2020
Metabolic reprogramming by N‐acetyl‐seryl‐aspartyl‐lysyl‐proline protects against diabetic kidney disease
Srivastava SP, Goodwin JE, Kanasaki K, Koya D. Metabolic reprogramming by N‐acetyl‐seryl‐aspartyl‐lysyl‐proline protects against diabetic kidney disease. British Journal Of Pharmacology 2020, 177: 3691-3711. PMID: 32352559, PMCID: PMC7393199, DOI: 10.1111/bph.15087.Peer-Reviewed Original ResearchConceptsACE inhibitorsDiabetic kidneyKidney fibrosisEffects of ACEIsEnd-stage renal diseaseDiabetic CD-1 miceKidney cell metabolismAbnormal glucose metabolismDiabetic kidney diseaseFirst-line drugsCD-1 miceMesenchymal transformationFatty acid oxidationMitochondrial fatty acid oxidationAntifibrotic mediatorsFatty acid metabolismDiabetic patientsRenal diseaseAntifibrotic mechanismsSevere fibrosisACE inhibitionKidney diseaseAntifibrotic actionReceptor antagonistC57BL6 miceCancer Biology and Prevention in Diabetes
Srivastava SP, Goodwin JE. Cancer Biology and Prevention in Diabetes. Cells 2020, 9: 1380. PMID: 32498358, PMCID: PMC7349292, DOI: 10.3390/cells9061380.Peer-Reviewed Original ResearchConceptsDPP-4 inhibitorsMesenchymal transitionType II diabetes mellitusCancer biologySite-specific cancersDevelopment of hyperglycemiaAnti-diabetic therapyRisk of cancerDipeptidyl peptidase-4New therapeutic approachesPossible mechanistic linkMolecular pathological mechanismsDiabetes mellitusSGLT2 inhibitorsChronic inflammationCancer-causing mechanismsDiabetic conditionsTumor cell extravasationAntidiabetic drugsTherapeutic approachesEpidemiological dataPeptidase-4DiabetesPathological mechanismsGlucocorticoid receptorInhibition of Angiotensin-Converting Enzyme Ameliorates Renal Fibrosis by Mitigating DPP-4 Level and Restoring Antifibrotic MicroRNAs
Srivastava SP, Goodwin JE, Kanasaki K, Koya D. Inhibition of Angiotensin-Converting Enzyme Ameliorates Renal Fibrosis by Mitigating DPP-4 Level and Restoring Antifibrotic MicroRNAs. Genes 2020, 11: 211. PMID: 32085655, PMCID: PMC7074526, DOI: 10.3390/genes11020211.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin Receptor AntagonistsAngiotensin-Converting Enzyme InhibitorsAnimalsCell LineDiabetes Mellitus, ExperimentalDiabetic NephropathiesDipeptidyl Peptidase 4Disease Models, AnimalDrug SynergismGene Expression RegulationHumansMiceMicroRNAsOligopeptidesSignal TransductionTransforming Growth Factor betaConceptsAngiotensin II receptor blockersRenal fibrosisDPP-4End-stage renal diseaseSubstrates of ACEDiabetic kidney diseaseEffect of ACEIII receptor blockersDPP-4 levelsTGFβ signalingAngiotensin converting enzymeChronic nephropathyReceptor blockersRenal diseaseKidney diseaseACEIEnzyme inhibitorsConventional drugsDownregulated expressionEndothelial cellsFibrosisInhibitory effectDrug 1MiR-29AcSDKP
2019
The Glucocorticoid Receptor in Cardiovascular Health and Disease
Liu B, Zhang TN, Knight JK, Goodwin JE. The Glucocorticoid Receptor in Cardiovascular Health and Disease. Cells 2019, 8: 1227. PMID: 31601045, PMCID: PMC6829609, DOI: 10.3390/cells8101227.Peer-Reviewed Original ResearchConceptsGlucocorticoid receptorGlucocorticoid signalingCardiovascular systemNon-genomic pathwaysClinical outcomesExogenous glucocorticoidsGlucocorticoid treatmentCardiovascular healthCardiovascular diseaseNuclear receptor familyTherapeutic strategiesAnimal modelsSteroid hormone cortisolHormone cortisolPathological conditionsReceptorsDiseaseReceptor familySignalingDistinct gene networksHuman diseasesDirect effectCritical roleInflammationPrognosisRole of the glucocorticoid receptor in glomerular disease
Goodwin JE. Role of the glucocorticoid receptor in glomerular disease. American Journal Of Physiology. Renal Physiology 2019, 317: f133-f136. PMID: 31166704, PMCID: PMC6692724, DOI: 10.1152/ajprenal.00217.2019.Peer-Reviewed Original ResearchConceptsGlomerular diseasePotent anti-inflammatory agentSteroid delivery systemsAnti-inflammatory agentsSystemic steroidsBeneficial direct effectsUnfavorable riskSystemic administrationTherapeutic benefitGlucocorticoid receptorRisk assessment algorithmClinicians' effortsBenefit ratioVivo studiesGlucocorticoidsDiseasePersonalized medicineDirect effectDelivery systemGlomeruliSteroidsAdministrationPodocytesReceptors
2018
SIRT3 deficiency leads to induction of abnormal glycolysis in diabetic kidney with fibrosis
Srivastava SP, Li J, Kitada M, Fujita H, Yamada Y, Goodwin JE, Kanasaki K, Koya D. SIRT3 deficiency leads to induction of abnormal glycolysis in diabetic kidney with fibrosis. Cell Death & Disease 2018, 9: 997. PMID: 30250024, PMCID: PMC6155322, DOI: 10.1038/s41419-018-1057-0.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarnitine O-PalmitoyltransferaseCell LineDiabetes Mellitus, ExperimentalDiabetic NephropathiesFibrosisGene Knockdown TechniquesGlucoseGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitKidneyMiceMice, Inbred C57BLPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPyruvate KinaseSirtuin 3StreptozocinTransfectionTransforming Growth Factor beta2ConceptsDiabetic kidneyAbnormal glycolysisAberrant glycolysisSIRT3 suppressionMouse modelProgressive diabetic kidney diseaseDiabetic kidney diseaseDiabetic mouse modelAberrant glucose metabolismSIRT3 protein levelsSIRT3 siRNADiabetic miceKidney diseaseKidney fibrosisSystemic administrationFibrogenic pathwaysSIRT3 deficiencyGlucose metabolismTherapeutic targetFibrosisSIRT3 levelsHIF1α accumulationFibrogenic phenotypeKidneyGrowth factor
2015
Glucocorticoids and the Cardiovascular System
Goodwin JE. Glucocorticoids and the Cardiovascular System. Advances In Experimental Medicine And Biology 2015, 872: 299-314. PMID: 26216000, DOI: 10.1007/978-1-4939-2895-8_13.Peer-Reviewed Original Research
2013
Abdominal distention and renal failure in a neonate
Bedri B, Goodwin JE. Abdominal distention and renal failure in a neonate. BMJ Case Reports 2013, 2013: bcr2012007955. PMID: 23429016, PMCID: PMC3604299, DOI: 10.1136/bcr-2012-007955.Peer-Reviewed Original ResearchConceptsAbdominal distentionRenal failureSevere unilateral hydronephrosisSignificant abdominal distentionPosterior urethral valvesTerm male neonateHospital dischargeUnilateral hydronephrosisUrethral valvesMale neonatePrenatal careDefinitive diagnosisMetabolic acidosisEchogenic kidneysDistentionNeonatesCystourethrogramHydronephrosisFailureDerangementAcidosisPediatriciansKidneyLab testsDiagnosisA 7-year-old boy with renal insufficiency and proteinuria after stem cell transplant for T-cell acute lymphoblastic leukemia
Goodwin JE, Palmer M, Pashankar F, Tufro A, Moeckel G. A 7-year-old boy with renal insufficiency and proteinuria after stem cell transplant for T-cell acute lymphoblastic leukemia. Clinical Nephrology 2013, 82: 205-210. PMID: 23391318, PMCID: PMC6990651, DOI: 10.5414/cn107767.Peer-Reviewed Original ResearchConceptsStem cell transplantHematopoietic stem cell transplantCell transplantRenal insufficiencyKidney biopsyPediatric patientsNephrotic syndromeExtensive foot process effacementAbnormal lymphocyte responsesT-cell acute lymphoblastic leukemiaChronic kidney diseaseChronic interstitial nephritisAcute lymphoblastic leukemiaPre-conditioning regimensFoot process effacementHost diseaseImmunosuppressive therapyRenal failureInterstitial nephritisLymphocyte responsesCommon sequelaeInterstitial infiltratesProphylactic medicationKidney diseaseLikely multifactorial
2012
Endothelial glucocorticoid receptor is required for protection against sepsis
Goodwin JE, Feng Y, Velazquez H, Sessa WC. Endothelial glucocorticoid receptor is required for protection against sepsis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2012, 110: 306-311. PMID: 23248291, PMCID: PMC3538225, DOI: 10.1073/pnas.1210200110.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCorticosteroneEndotheliumGene DeletionHemodynamicsHuman Umbilical Vein Endothelial CellsHumansIn Situ Nick-End LabelingInterleukin-6LipopolysaccharidesMaleMiceMice, KnockoutNF-kappa BNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIReceptors, GlucocorticoidSepsisTumor Necrosis Factor-alphaConceptsEndothelial nitric oxide synthaseEndothelial glucocorticoid receptorHuman umbilical vein cellsGlucocorticoid receptorInterleukin-6Inducible nitric oxide synthase (iNOS) expressionExpression of eNOSNitric oxide synthase expressionHigher nitric oxide levelsOxide synthase expressionNitric oxide levelsNF-κB levelsSpecific iNOS inhibitorNitric oxide synthaseNitric oxide synthesisNF-κB activationRate of apoptosisHemodynamic collapseHemodynamic instabilityTissue-specific deletionUmbilical vein cellsInflammatory cytokinesINOS inhibitorTumor necrosisOxide synthase
2011
Glucocorticoid-induced hypertension
Goodwin JE, Geller DS. Glucocorticoid-induced hypertension. Pediatric Nephrology 2011, 27: 1059-1066. PMID: 21744056, DOI: 10.1007/s00467-011-1928-4.BooksConceptsGlucocorticoid-induced hypertensionForms of hypertensionGlucocorticoid receptorRenal mineralocorticoid receptorsCommon clinical problemVascular smooth muscleBlood pressure regulationVascular endothelial cellsTissue-specific contributionsMineralocorticoid receptorTreatment strategiesClinical dataHypertensionSmooth muscleClinical problemAnimal modelsKidney tissuePressure regulationOrgan systemsWater reabsorptionEndothelial cellsExtra-vascular tissuesReceptorsPathogenesisMouse genetics
2008
Characterization of a Novel Gain of Function Glucocorticoid Receptor Knock-in Mouse*
Zhang J, Ge R, Matte-Martone C, Goodwin J, Shlomchik WD, Mamula MJ, Kooshkabadi A, Hardy MP, Geller D. Characterization of a Novel Gain of Function Glucocorticoid Receptor Knock-in Mouse*. Journal Of Biological Chemistry 2008, 284: 6249-6259. PMID: 19017639, PMCID: PMC2649105, DOI: 10.1074/jbc.m807997200.Peer-Reviewed Original ResearchConceptsHuman glucocorticoid receptorStudies of glucocorticoidsAdrenocortical sizeGR altersEndogenous glucocorticoidsACTH levelsAdrenal axisReceptor knockImmunologic studiesWild-type GRMaintenance of homeostasisCorticosterone levelsGlucocorticoid receptorGlucocorticoidsNovel gainPhysiologic functionMicePathological processesMutant GRGC functionBasal regulationVivoGC physiologyHomologous recombinationHuman diseases