2022
Effect of pulsed intravenous methylprednisolone with alternative low-dose prednisone on high-risk IgA nephropathy: a 18-month prospective clinical trial
Li Y, Fu R, Gao J, Wang L, Duan Z, Tian L, Ge H, Ma X, Zhang Y, Li K, Xu P, Tian X, Chen Z. Effect of pulsed intravenous methylprednisolone with alternative low-dose prednisone on high-risk IgA nephropathy: a 18-month prospective clinical trial. Scientific Reports 2022, 12: 255. PMID: 34996948, PMCID: PMC8742122, DOI: 10.1038/s41598-021-03691-0.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, IntravenousAdministration, OralAdultDisease ProgressionDrug TaperingDrug Therapy, CombinationFemaleGlomerulonephritis, IGAGlucocorticoidsHumansKidney Failure, ChronicMaleMethylprednisolonePrednisoneProspective StudiesProteinuriaPulse Therapy, DrugRemission InductionRisk AssessmentRisk FactorsTime FactorsTreatment OutcomeConceptsLow-dose prednisoneComplete remissionFP groupIntravenous methylprednisoloneHigh-risk IgA nephropathyOxford MEST-C scoreChinese Clinical Trial RegistryPulsed intravenous methylprednisoloneACEI/ARBClinical Trials RegistryProspective clinical trialsMEST-C scoreFavorable safety profilePercentage of CROral prednisoneTotal remissionAdult patientsNephropathy patientsPrednisone regimenCushing's syndromeMore patientsPrimary outcomeTrials RegistryClinical outcomesIgA nephropathy
2021
Distinct Roles of Type I and Type III Interferons during a Native Murine β Coronavirus Lung Infection
Sharma L, Peng X, Qing H, Hilliard BK, Kim J, Swaminathan A, Tian J, Israni-Winger K, Zhang C, Habet V, Wang L, Gupta G, Tian X, Ma Y, Shin HJ, Kim SH, Kang MJ, Ishibe S, Young LH, Kotenko S, Compton S, Wilen CB, Wang A, Dela Cruz CS. Distinct Roles of Type I and Type III Interferons during a Native Murine β Coronavirus Lung Infection. Journal Of Virology 2021, 96: e01241-21. PMID: 34705554, PMCID: PMC8791255, DOI: 10.1128/jvi.01241-21.Peer-Reviewed Original ResearchConceptsType I interferonType III interferonsI interferonIII interferonsCoronavirus infectionInterferon deficiencyViral clearanceViral loadLung infectionType IHealthy young patientsImproved host survivalHost survivalRole of interferonMurine coronavirus infectionMajor health care threatViral burdenYounger patientsEarly diseaseIntranasal routeInterferon treatmentSublethal infectionEarly treatmentLethal infectionTissue injuryAMP-Kinase mediates regulation of glomerular volume and podocyte survival
Banu K, Lin Q, Basgen JM, Planoutene M, Wei C, Reghuvaran AC, Tian X, Shi H, Garzon F, Garzia A, Chun N, Cumpelik A, Santeusanio AD, Zhang W, Das B, Salem F, LI L, Ishibe S, Cantley LG, Kaufman L, Lemley KV, Ni Z, He JC, Murphy B, Menon MC. AMP-Kinase mediates regulation of glomerular volume and podocyte survival. JCI Insight 2021, 6: e150004. PMID: 34473647, PMCID: PMC8525649, DOI: 10.1172/jci.insight.150004.Peer-Reviewed Original ResearchAdenylate KinaseAdolescentAdultAgedAlbuminuriaAnimalsCell SizeCell SurvivalChildChild, PreschoolFemaleGene Knockdown TechniquesGlomerulonephritis, MembranousGlomerulosclerosis, Focal SegmentalHumansHypertrophyInfantKidney GlomerulusMaleMiceMicrofilament ProteinsMiddle AgedNephrectomyNephrosis, LipoidNephrotic SyndromePodocytesProportional Hazards ModelsProto-Oncogene Proteins c-fynYoung AdultProfibrotic mechanisms of DPP8 and DPP9 highly expressed in the proximal renal tubule epithelial cells
Zhang Y, Li K, Li Y, Zhao W, Wang L, Chen Z, Ma X, Yao T, Wang J, Dong W, Li X, Tian X, Fu R. Profibrotic mechanisms of DPP8 and DPP9 highly expressed in the proximal renal tubule epithelial cells. Pharmacological Research 2021, 169: 105630. PMID: 33932609, DOI: 10.1016/j.phrs.2021.105630.Peer-Reviewed Original ResearchMeSH KeywordsAdamantaneAnimalsBlotting, WesternCase-Control StudiesCell LineDipeptidasesDipeptidesDipeptidyl-Peptidases and Tripeptidyl-PeptidasesEpithelial-Mesenchymal TransitionFibrosisFluorescent Antibody TechniqueHumansKidney Tubules, ProximalMaleMiceMice, Inbred C57BLReal-Time Polymerase Chain ReactionRenal Insufficiency, ChronicConceptsTubulointerstitial fibrosisTubule epithelial cellsCKD patientsUUO miceHK-2 cell modelChronic kidney disease patientsTGF-β1/Smad signalingUnilateral ureteral obstruction animal modelEpithelial cellsKidney disease patientsHealthy control subjectsKidney biopsy specimensProximal tubule epithelial cellsRenal tubule epithelial cellsRenal proximal tubule epithelial cellsHK-2 cellsPotential therapeutic targetRenal inflammationTubulointerstitial injuryRenal functionUUO groupKidney functionProfibrotic mechanismsControl subjectsDisease patients
2020
Inhibiting calpain 1 and 2 in cyclin G associated kinase–knockout mice mitigates podocyte injury
Tian X, Inoue K, Zhang Y, Wang Y, Sperati CJ, Pedigo CE, Zhao T, Yan M, Groener M, Moledina DG, Ebenezer K, Li W, Zhang Z, Liebermann D, Greene L, Greer P, Parikh CR, Ishibe S. Inhibiting calpain 1 and 2 in cyclin G associated kinase–knockout mice mitigates podocyte injury. JCI Insight 2020, 5: e142740. PMID: 33208557, PMCID: PMC7710277, DOI: 10.1172/jci.insight.142740.Peer-Reviewed Original ResearchConceptsCalpain-1Chronic kidney diseaseDegree of proteinuriaCalpain inhibitor IIIGlomeruli of patientsProgressive proteinuriaCalpain protease activityGlobal glomerulosclerosisGlomerular injuryKidney functionKidney diseaseKidney failureCalcium dysregulationPodocyte injuryPodocyte-specific deletionPodocyte damageG associated kinaseProtective roleCalpain activationProteinuriaGlomerulosclerosisMiceReduced expressionStriking increaseInjuryDynamin 1 is important for microtubule organization and stabilization in glomerular podocytes
La TM, Tachibana H, Li S, Abe T, Seiriki S, Nagaoka H, Takashima E, Takeda T, Ogawa D, Makino S, Asanuma K, Watanabe M, Tian X, Ishibe S, Sakane A, Sasaki T, Wada J, Takei K, Yamada H. Dynamin 1 is important for microtubule organization and stabilization in glomerular podocytes. The FASEB Journal 2020, 34: 16449-16463. PMID: 33070431, DOI: 10.1096/fj.202001240rr.Peer-Reviewed Original ResearchConceptsDynamin 1Microtubule organizationMouse podocytesΑ-tubulinMicrotubule bundlesGlomerular podocytesEndocytic proteinsMicrotubule bundle formationStabilization of microtubulesAcetylated α-tubulinVesicle formationNocodazole resistanceImmunoelectron microscopyMicrotubulesPhysiological significanceBundle formationRat podocytesProtective Role of Tangshen Formula on the Progression of Renal Damage in db/db Mice by TRPC6/Talin1 Pathway in Podocytes
Wang Q, Tian X, Zhou W, Wang Y, Zhao H, Li J, Zhou X, Zhang H, Zhao T, Li P. Protective Role of Tangshen Formula on the Progression of Renal Damage in db/db Mice by TRPC6/Talin1 Pathway in Podocytes. Journal Of Diabetes Research 2020, 2020: 3634974. PMID: 33015191, PMCID: PMC7519445, DOI: 10.1155/2020/3634974.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCell AdhesionCell MovementCell SurvivalCytoskeletonDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Disease ProgressionDrugs, Chinese HerbalHumansKidney DiseasesKidney GlomerulusMaleMedicine, Chinese TraditionalMiceMice, Inbred C57BLPodocytesProteinuriaTalinTRPC6 Cation ChannelWound HealingConceptsDiabetic kidney diseasePrimary mouse podocytesTangshen FormulaTransient receptor potential canonical channel 6Renal functionKidney diseaseTSF treatmentMouse podocytesType 2 diabetic kidney diseaseProtective roleDb/db miceAdvanced glycation end productsTRPC6-dependent CaProteinuric kidney diseaseActivated T cells 2Chinese medicine formulaGlycation end productsExpression of Talin1T cells 2Foot process effacementLoss of talin1Renal damageDb micePodocyte numberMurine modelEstablishment of a novel nomogram for the clinically diagnostic prediction of minimal change disease, −a common cause of nephrotic syndrome
Yan G, Liu G, Tian X, Tian L, Wang H, Ren P, Ma X, Fu R, Chen Z. Establishment of a novel nomogram for the clinically diagnostic prediction of minimal change disease, −a common cause of nephrotic syndrome. BMC Nephrology 2020, 21: 396. PMID: 32928127, PMCID: PMC7490860, DOI: 10.1186/s12882-020-02058-3.Peer-Reviewed Original ResearchMeSH KeywordsAdultArea Under CurveBlood PressureComplement C1qComplement C3Complement C4DiastoleFemaleGlomerular Filtration RateHemoglobinsHumansImmunoglobulin EImmunoglobulin GImmunoglobulin MMaleMiddle AgedNephrosis, LipoidNephrotic SyndromeNomogramsRegression AnalysisReproducibility of ResultsSensitivity and SpecificityYoung AdultConceptsDiastolic blood pressurePrimary glomerular diseaseNephrotic syndromeAdult patientsRenal biopsyChange diseaseGlomerular diseaseBackgroundMinimal change diseaseMinimal change diseaseLASSO regression analysisRenal biopsy procedureNon-MCD groupLogistic regression modelsDiagnostic prediction modelNovel nomogramPatient demographicsBlood pressureSerum levelsOverall incidenceClinical manifestationsMCD patientsMCD diagnosisCommon causeInvasive proceduresMethodA total
2019
Inhibition of Endocytosis of Clathrin-Mediated Angiotensin II Receptor Type 1 in Podocytes Augments Glomerular Injury
Inoue K, Tian X, Velazquez H, Soda K, Wang Z, Pedigo CE, Wang Y, Cross E, Groener M, Shin JW, Li W, Hassan H, Yamamoto K, Mundel P, Ishibe S. Inhibition of Endocytosis of Clathrin-Mediated Angiotensin II Receptor Type 1 in Podocytes Augments Glomerular Injury. Journal Of The American Society Of Nephrology 2019, 30: 2307-2320. PMID: 31511362, PMCID: PMC6900791, DOI: 10.1681/asn.2019010053.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAlbuminuriaAngiotensin IIAnimalsCalcium SignalingCells, CulturedClathrin-Coated VesiclesCreatinineDynamin IDynamin IIEndocytosisGlomerulonephritisHemodynamicsKidney GlomerulusMaleMiceMice, KnockoutNeuropeptidesPodocytesPseudopodiaRac1 GTP-Binding ProteinReceptor, Angiotensin, Type 1ConceptsDouble knockout miceAngiotensin II receptor type 1Receptor type 1Renin-angiotensin system blockersType 1Renin-angiotensin systemPrimary podocytesEffects of AngIIImproved albuminuriaSystem blockersGlomerular hyperfiltrationGlomerular filtration barrierGlomerular injuryKidney functionAngiotensin IIKidney failurePodocyte injuryProtective effectCalcium influxRac1 activationAngII stimulationMice exhibitAngIIGenetic ablationMiceProtective effects of GPR120 agonist-programmed macrophages on renal interstitial fibrosis in unilateral ureteral obstruction (UUO) rats
Wang L, Ren X, Tian XF, Cheng XL, Zhao YY, Li QY, Duan ZY, Tian LF, Chen Z, Lu JM, Liang XY, Zhao YF, Fu RG. Protective effects of GPR120 agonist-programmed macrophages on renal interstitial fibrosis in unilateral ureteral obstruction (UUO) rats. Biomedicine & Pharmacotherapy 2019, 117: 109172. PMID: 31261028, DOI: 10.1016/j.biopha.2019.109172.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBeta CateninBiphenyl CompoundsCytokinesFibrosisGene Expression RegulationKidney DiseasesMacrophages, PeritonealMaleModels, BiologicalPhenotypePhenylpropionatesProtective AgentsRats, Sprague-DawleyReceptors, G-Protein-CoupledSignal TransductionTransforming Growth Factor beta1Ureteral ObstructionVimentinConceptsRenal interstitial fibrosisUnilateral ureteral obstructionInterstitial fibrosisUreteral obstructionProtective effectFree fatty acid receptor GPR120Fatty acid receptor GPR120Unilateral ureteral obstruction operationPeritoneal macrophagesAbnormal expressionExpression of CD206M2 phenotype macrophagesTumor necrosis factorEpithelial-mesenchymal transitionAutologous administrationReceptor GPR120UUO ratsInterleukin-6Intrarenal injectionArginase-1Necrosis factorGPR120 agonistM2 phenotypeΑ-SMATGF-β1Podocyte histone deacetylase activity regulates murine and human glomerular diseases
Inoue K, Gan G, Ciarleglio M, Zhang Y, Tian X, Pedigo CE, Cavanaugh C, Tate J, Wang Y, Cross E, Groener M, Chai N, Wang Z, Justice A, Zhang Z, Parikh CR, Wilson FP, Ishibe S. Podocyte histone deacetylase activity regulates murine and human glomerular diseases. Journal Of Clinical Investigation 2019, 129: 1295-1313. PMID: 30776024, PMCID: PMC6391095, DOI: 10.1172/jci124030.Peer-Reviewed Original ResearchConceptsEarly growth response 1Histone deacetylase 1Proteinuric patientsKidney diseaseHDAC2 activityValproic acidVeterans Aging Cohort StudyEnd-stage kidney diseaseDegree of proteinuriaGlomerular filtration rateAging Cohort StudyInhibition of HDAC1Proteinuric kidney diseaseHuman glomerular diseasesGlomerular disease modelsConnectivity Map databaseCohort studyFiltration rateGlomerular diseaseHistone deacetylase activityProteinuric kidneysHDAC inhibitorsProteinuriaMRNA expressionGenetic ablation
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