grant

Pax8-Hnf4a co-regulation in ischemic kidney injury

Organization UNIVERSITY OF MICHIGAN AT ANN ARBORLocation ANN ARBOR, UNITED STATESPosted 11 Aug 2024Deadline 31 Jul 2026
NIHUS FederalResearch GrantFY2025Acute Kidney FailureAcute Kidney InsufficiencyAcute Renal FailureAcute Renal InsufficiencyAffectAwardBasal Transcription FactorBasal transcription factor genesBindingBleedingCarbonCell BodyCell RespirationCellsCellular RespirationChromatinClinicalDNA BindingDNA Binding InteractionDNA boundDataDevelopmentEnhancer ElementsEpitheliumFatty Acid Metabolism PathwayFoundationsFreezingGene TranscriptionGeneral Transcription Factor GeneGeneral Transcription FactorsGenesGeneticGenetic DeterminismGenetic Enhancer ElementGenetic TranscriptionGoalsHNF4HNF4-AlphaHNF4AHNF4A geneHemorrhageHepatocyte Nuclear Factor 4-AlphaHepatocyte Nuclear Factor, 4Hospital AdmissionHospitalizationInjuryInjury to KidneyIntermediary MetabolismIschemiaIschemia-Reperfusion InjuryKidneyKidney Urinary SystemMeasuresMediatingMetabolicMetabolic PathwayMetabolic ProcessesMetabolismMiceMice MammalsMichiganModelingMolecularMolecular InteractionMorbidityMorbidity - disease rateMurineMusNephronsPathogenesisPathway interactionsPatientsPatternPopulationProcessRNA ExpressionRecommendationRegulationRenal CellReperfusion DamageReperfusion InjuryResearchResearch SupportResistanceRiskRoleSamplingSiteSpecificitySyndromeTCF14TestingTextTissue SampleToxic effectToxicitiesTranscriptionTranscription Factor 14, Hepatic Nuclear FactorTranscription Factor Proto-OncogeneTranscription factor genesUniversitiesUriniferous TubeVascular blood supplyacute kidney injuryaerobic metabolismaerobic respirationblood lossblood supplyclinical practicecostdevelopmentalenhancer sequenceexperimentexperimental researchexperimental studyexperimentsfatty acid metabolismgenetic determinantgenetic enhancer sequenceglobal gene expressionglobal transcription profilein vivoinjuriesischemia injuryischemic injurykidney cellkidney cortexkidney cortical portionkidney injurykidney ischemiametabolic profilemetabolism measurementmetabolomicsmetabonomicsmitochondrial dysfunctionmortalitymutantnew drug targetnew druggable targetnew pharmacotherapy targetnew therapeutic targetnew therapy targetnovelnovel drug targetnovel druggable targetnovel pharmacotherapy targetnovel therapeutic targetnovel therapy targetoxidative metabolismpathwaypreventpreventingprogramsrenalrenal cortexrenal injuryrenal ischemiaresistantresponserisk stratificationsocial rolesolutestratify risktooltranscription factortranscriptometranscriptomicsvascular supply
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Full Description

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The goals of this project are to 1) test the hypothesis that Pax8 expression controls sensitivity to ischemic kidney injury in the mature proximal tubule by promoting transcription of Hnf4a targets and 2) facilitate a path to an independent research program for the PI. Ischemic acute kidney injury (AKI) is a common clinical syndrome associated with significant mortality, yet no treatments are in routine clinical use. Ischemic AKI most strongly affects the proximal tubule, in part due to the unique metabolic pathways used by this nephron segment. Understanding the molecular and genetic mechanisms that establish this unique metabolic profile could lead to a better understanding of ischemic AKI pathogenesis and new therapeutic targets. As part of the associated K08 award, we discovered that proximal-tubule-selective depletion of the transcription factor Pax8 resulted in a population of proximal tubule cells resistant to kidney injury. Analysis of the transcriptome of these cells revealed alterations in genes associated with proximal tubule metabolism. However, the genes affected by Pax8 depletion were not preferentially associated with sites of Pax8 chromatin binding. Analysis of other transcription factors associated with genes affected by Pax8 depletion revealed a central role of Hnf4a. These observations suggest the hypothesis that Pax8 expression controls sensitivity to ischemic kidney injury in the proximal tubule by promoting transcription of Hnf4a targets. This project will investigate this hypothesis by determining the role of Pax8 in the chromatin localization of Hnf4a and by identifying metabolic pathways coregulated by Pax8 and HNF4a in response to ischemic injury in vivo. The targets identified in each of these aims will form the basis for independent research support studying the molecular and genetic determinants of ischemic AKI risk.

Grant Number: 5R03DK140216-02
NIH Institute/Center: NIH

Principal Investigator: Jeffrey Beamish

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Pax8-Hnf4a co-regulation in ischemic kidney injury — UNIVERSITY OF MICHIGAN AT ANN ARBOR | UNITED STATES | Aug 2024 | Dev Procure