2021
Podocyte Glucocorticoid Receptors Are Essential for Glomerular Endothelial Cell Homeostasis in Diabetes Mellitus
Srivastava SP, Zhou H, Setia O, Dardik A, Fernandez‐Hernando C, Goodwin J. Podocyte Glucocorticoid Receptors Are Essential for Glomerular Endothelial Cell Homeostasis in Diabetes Mellitus. Journal Of The American Heart Association 2021, 10: e019437. PMID: 34308664, PMCID: PMC8475689, DOI: 10.1161/jaha.120.019437.Peer-Reviewed Original ResearchConceptsDiabetic nephropathySegmental fibrosisFatty acid metabolismDiabetes mellitusEndothelial cellsPrimary podocytesReceptor knockout micePathogenesis of proteinuriaAdministration of streptozotocinProfibrotic gene expressionAcid metabolismGlomerular endothelial cellsSmooth muscle actinEndothelial cell homeostasisCarnitine palmitoyltransferase 1AFatty acid oxidationBackground ProteinuriaWorsened fibrosisClinical characteristicsFibrotic featuresGlomerular fibrosisGlomerular homeostasisPatient managementControl littermatesSevere disease
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
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