2020
Polycystin 2 is increased in disease to protect against stress-induced cell death
Brill AL, Fischer TT, Walters JM, Marlier A, Sewanan LR, Wilson PC, Johnson EK, Moeckel G, Cantley LG, Campbell SG, Nerbonne JM, Chung HJ, Robert ME, Ehrlich BE. Polycystin 2 is increased in disease to protect against stress-induced cell death. Scientific Reports 2020, 10: 386. PMID: 31941974, PMCID: PMC6962458, DOI: 10.1038/s41598-019-57286-x.Peer-Reviewed Original ResearchConceptsPolycystin-2General cellular homeostasisCell deathStress-induced cell deathPathological cell deathAutosomal dominant polycystic kidney diseaseEndoplasmic reticulum membraneCellular homeostasisCellular stressPrimary ciliaUbiquitous expressionExpression changesCell stressReticulum membraneTransient receptor potential cation channelHuman diseasesMultiple tissuesEndogenous roleDominant polycystic kidney diseaseTissue typesCation channelsPolycystic kidney diseaseDifferent pathological statesMultiple diseasesKidney disease
2018
The protective role of macrophage migration inhibitory factor in acute kidney injury after cardiac surgery
Stoppe C, Averdunk L, Goetzenich A, Soppert J, Marlier A, Kraemer S, Vieten J, Coburn M, Kowark A, Kim BS, Marx G, Rex S, Ochi A, Leng L, Moeckel G, Linkermann A, El Bounkari O, Zarbock A, Bernhagen J, Djudjaj S, Bucala R, Boor P. The protective role of macrophage migration inhibitory factor in acute kidney injury after cardiac surgery. Science Translational Medicine 2018, 10 PMID: 29769287, DOI: 10.1126/scitranslmed.aan4886.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAnimalsAntigens, Differentiation, B-LymphocyteAntioxidantsCardiac Surgical ProceduresCell DeathHistocompatibility Antigens Class IIHumansIncidenceInflammationKidneyLipid PeroxidationLipocalin-2Macrophage Migration-Inhibitory FactorsMice, Inbred C57BLOxidative StressProtective AgentsProtein DomainsRecombinant ProteinsReperfusion InjuryRhabdomyolysisConceptsMacrophage migration inhibitory factorAcute kidney injuryRecombinant macrophage migration inhibitory factorIschemia-reperfusion injuryCardiac surgeryMigration inhibitory factorTubular epithelial cellsKidney injuryHigher macrophage migration inhibitory factorIncidence of AKIPathogenesis of AKIUrinary Macrophage Migration Inhibitory FactorExperimental acute kidney injuryExperimental ischemia-reperfusion injuryInhibitory factorMyocardial ischemia-reperfusion injuryOxidative stressMIF serum concentrationsCardiac surgery patientsRenal tubular epithelial cellsConventional cardiac surgeryEpithelial cellsHours of reperfusionSetting of hypoxiaTubular cell injury
2006
Glomerular injury is exacerbated in diabetic integrin α1-null mice
Zent R, Yan X, Su Y, Hudson B, Borza D, Moeckel G, Qi Z, Sado Y, Breyer M, Voziyan P, Pozzi A. Glomerular injury is exacerbated in diabetic integrin α1-null mice. Kidney International 2006, 70: 460-470. PMID: 16775606, DOI: 10.1038/sj.ki.5000359.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBasement MembraneCell DivisionCell MovementCells, CulturedCollagen Type IVDiabetes Mellitus, ExperimentalDiabetic NephropathiesDisease Models, AnimalGlomerular Filtration RateGlucoseGlycation End Products, AdvancedIntegrin alpha1Integrin alpha1beta1MaleMesangial CellsMiceMice, Inbred BALB CMice, KnockoutOxidative StressReactive Oxygen SpeciesConceptsGlomerular filtration rateWild-type miceDiabetic wild-type miceDiabetic nephropathyGlomerular injuryCollagen depositionMesangial cellsGlomerular basement membrane thickeningCollagen IVGlomerular collagen IVIntegrin alpha1-null miceNon-diabetic miceIntegrin α1-null miceBasement membrane thickeningDiabetic mutant mouseGlomerular collagen depositionROS productionCollagen IV productionSTZ injectionWeek 24Renal diseaseGlomerular depositionWeek 36Week 12Filtration rate