2023
Loss of endothelial glucocorticoid receptor accelerates organ fibrosis in db/db mice
Srivastava S, Goodwin J. Loss of endothelial glucocorticoid receptor accelerates organ fibrosis in db/db mice. American Journal Of Physiology. Renal Physiology 2023, 325: f519-f526. PMID: 37589053, PMCID: PMC10639025, DOI: 10.1152/ajprenal.00105.2023.Peer-Reviewed Original ResearchConceptsEndothelial glucocorticoid receptorGlucocorticoid receptorOrgan fibrosisMouse modelMultiple organsSpontaneous type 2 diabetesDb/db miceDiabetic kidney fibrosisReceptor-mediated upregulationUse of metforminDiabetic renal fibrosisType 2 diabetesMechanisms of fibrosisGenetic mouse modelsUpregulation of WntRenal fibrosisSevere fibrosisDb miceIL-6Key cytokineKidney fibrosisDisease processFibrosisFibrotic conditionsWnt inhibitors
2020
Endothelial cell–glucocorticoid receptor interactions and regulation of Wnt signaling
Zhou H, Mehta S, Srivastava SP, Grabinska K, Zhang X, Wong C, Hedayat A, Perrotta P, Fernández-Hernando C, Sessa WC, Goodwin JE. Endothelial cell–glucocorticoid receptor interactions and regulation of Wnt signaling. JCI Insight 2020, 5: e131384. PMID: 32051336, PMCID: PMC7098785, DOI: 10.1172/jci.insight.131384.Peer-Reviewed Original ResearchConceptsEndothelial glucocorticoid receptorVascular inflammationGlucocorticoid receptorGlucocorticoid receptor regulationGlucocorticoid receptor resultsUpregulation of WntEndogenous glucocorticoidsExogenous glucocorticoidsGlucocorticoid response elementCardiovascular diseaseMouse endothelial cellsMouse modelEndothelial WNTInflammationReceptor regulationEndothelial cellsReceptors resultsNext-generation sequencingReceptor interactionReceptorsRegulation of WntWnt pathwayGlucocorticoidsRecent dataWnt
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
2017
Loss of the podocyte glucocorticoid receptor exacerbates proteinuria after injury
Zhou H, Tian X, Tufro A, Moeckel G, Ishibe S, Goodwin J. Loss of the podocyte glucocorticoid receptor exacerbates proteinuria after injury. Scientific Reports 2017, 7: 9833. PMID: 28852159, PMCID: PMC5575043, DOI: 10.1038/s41598-017-10490-z.Peer-Reviewed Original ResearchConceptsKnockout miceGlucocorticoid receptorNephrotic syndromeSimilar renal functionMainstay of therapyReceptor knockout miceTreatment of proteinuriaFoot process effacementMechanism of actionImmunomodulatory therapyRenal functionGlomerular injuryProtein excretionKO miceCommon disorderNephrotoxic serumPodocyte injuryPodocyte-specific deletionMouse modelSlit diaphragm proteinsWild-type podocytesProcess effacementProteinuriaUnstimulated conditionsKnockout animals
2011
Knockout of the vascular endothelial glucocorticoid receptor abrogates dexamethasone-induced hypertension
Goodwin JE, Zhang J, Gonzalez D, Albinsson S, Geller DS. Knockout of the vascular endothelial glucocorticoid receptor abrogates dexamethasone-induced hypertension. Journal Of Hypertension 2011, 29: 1347-1356. PMID: 21659825, PMCID: PMC3439131, DOI: 10.1097/hjh.0b013e328347da54.Peer-Reviewed Original ResearchConceptsEndothelial glucocorticoid receptorGlucocorticoid receptorMean blood pressure increaseKnockout animalsDexamethasone-induced hypertensionBlood pressure increaseCircadian BP rhythmForms of hypertensionEffects of glucocorticoidsNormal circadian BP rhythmPeripheral circadian clocksBaseline BPBP rhythmMmHg increaseContractile responseBP homeostasisResistance arteriolesTissue-specific knockoutFundamental physiologic processesDexamethasone treatmentHypertensionMouse modelControl animalsVascular endotheliumKnockout mice
2010
The glucocorticoid receptor in the distal nephron is not necessary for the development or maintenance of dexamethasone-induced hypertension
Goodwin JE, Zhang J, Velazquez H, Geller DS. The glucocorticoid receptor in the distal nephron is not necessary for the development or maintenance of dexamethasone-induced hypertension. Biochemical And Biophysical Research Communications 2010, 394: 266-271. PMID: 20188070, PMCID: PMC2946623, DOI: 10.1016/j.bbrc.2010.02.123.Peer-Reviewed Original ResearchConceptsGlucocorticoid-induced hypertensionGlucocorticoid receptorDistal nephronKnockout miceSimilar hypertensive responsesBaseline blood pressureDevelopment of hypertensionReceptor knockout miceAdministration of glucocorticoidsSimilar body weightGlucocorticoid receptor actionHypertensive responseRenal histologyBlood pressureUrinary excretionTissue-specific knockoutMineralocorticoid receptorHypertensionMouse modelLittermate controlsNephron numberSide effectsBody weightReceptor actionImportant mediator
2008
A Critical Role for Vascular Smooth Muscle in Acute Glucocorticoid-Induced Hypertension
Goodwin JE, Zhang J, Geller DS. A Critical Role for Vascular Smooth Muscle in Acute Glucocorticoid-Induced Hypertension. Journal Of The American Society Of Nephrology 2008, 19: 1291-1299. PMID: 18434569, PMCID: PMC2440298, DOI: 10.1681/asn.2007080911.Peer-Reviewed Original ResearchConceptsVascular smooth muscleAcute hypertensive responseHypertensive responseKO miceSmooth muscleGC receptorChronic hypertensive responseGlucocorticoid-Induced HypertensionNormal circadian variationBaseline BPTissue-specific knockoutMineralocorticoid receptorMouse modelHypertensionExcess reabsorptionCircadian variationCritical roleMiceReceptorsPromiscuous activationMuscleVivoKnockoutResponseGlucocorticoids