K+-induced HSP-72 expression is mediated via rapid Ca2+ influx in renal epithelial cells
Eickelberg O, Geibel J, Seebach F, Giebisch G, Kashgarian M. K+-induced HSP-72 expression is mediated via rapid Ca2+ influx in renal epithelial cells. American Journal Of Physiology. Renal Physiology 2001, 281: f280-f287. PMID: 11457719, DOI: 10.1152/ajprenal.2001.281.2.f280.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalciumCalcium Channel BlockersCell LineDiltiazemEgtazic AcidEnzyme InhibitorsEpithelial CellsGallic AcidGenes, ReporterHeat-Shock ProteinsHSP72 Heat-Shock ProteinsImmunoblottingKidney Tubules, ProximalMicroscopy, ConfocalPotassiumPromoter Regions, GeneticRecombinant Fusion ProteinsSodiumSwineThapsigarginUrotheliumConceptsHSP 72 expressionPromoter activityHSP 72Protein expressionProtective cellular responseLuciferase reporter geneHSP-25Heat shock protein expressionRenal epithelial cellsTranscriptional inductionShock protein expressionIonic stressReporter geneHSP-90 levelsHSC 73Cellular responsesChannel blocker diltiazemIntracellular lumenWestern blot analysisChelator EGTA-AMPathophysiological stimuliBlot analysisConfocal microscopyProtein levelsExtracellular spaceMolecular mechanisms of TGF‐β antagonism by interferon γ and cyclosporine A in lung fibroblasts
EICKELBERG O, PANSKY A, KOEHLER E, BIHL M, TAMM M, HILDEBRAND P, PERRUCHOUD A, KASHGARIAN M, ROTH M. Molecular mechanisms of TGF‐β antagonism by interferon γ and cyclosporine A in lung fibroblasts. The FASEB Journal 2001, 15: 797-806. PMID: 11259398, DOI: 10.1096/fj.00-0233com.Peer-Reviewed Original ResearchMeSH KeywordsCells, CulturedCollagenCyclosporineDNA-Binding ProteinsExtracellular MatrixFibroblastsGenes, ReporterHumansInterferon-gammaLungModels, BiologicalOligonucleotides, AntisenseProto-Oncogene Proteins c-junPulmonary FibrosisSignal TransductionSTAT1 Transcription FactorTrans-ActivatorsTranscription Factor AP-1Transforming Growth Factor betaConceptsCollagen depositionLung fibroblastsIFN-gammaExcess extracellular matrix depositionGrowth factor-beta activityPrimary human lung fibroblastsFibrotic lung diseaseHuman lung fibroblastsTGF-beta antagonismAP-1IFN-gamma treatmentExtracellular matrix depositionLung fibrosisFatal conditionLung diseaseMolecular mechanismsPathological featuresInterferon γTranscription factor AP-1Future therapiesPharmacological agentsJunD homodimersFactor AP-1Novel targetDirect inhibition