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
2014
Loss of the Endothelial Glucocorticoid Receptor Prevents the Therapeutic Protection Afforded by Dexamethasone after LPS
Goodwin JE, Feng Y, Velazquez H, Zhou H, Sessa WC. Loss of the Endothelial Glucocorticoid Receptor Prevents the Therapeutic Protection Afforded by Dexamethasone after LPS. PLOS ONE 2014, 9: e108126. PMID: 25299055, PMCID: PMC4191990, DOI: 10.1371/journal.pone.0108126.Peer-Reviewed Original ResearchConceptsKO miceLow-dose LPSSepsis-like syndromeAnti-inflammatory therapyInflammatory cytokines TNFKO mice showRegulation of NFNF-κB activationNitric oxide releaseTherapeutic protectionIL-6INOS productionCytokines TNFReceptor preventsIdentical doseControl animalsMice showGlucocorticoid receptorOxide releaseDexamethasoneLPSMiceProlonged activationActivationSepsis
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