2001
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 space
1999
Thresholds for cellular disruption and activation of the stress response in renal epithelia
van Why S, Kim S, Geibel J, Seebach F, Kashgarian M, Siegel N. Thresholds for cellular disruption and activation of the stress response in renal epithelia. American Journal Of Physiology 1999, 277: f227-f234. PMID: 10444577, DOI: 10.1152/ajprenal.1999.277.2.f227.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsCalciumCysteine EndopeptidasesDetergentsDifferential ThresholdDNA-Binding ProteinsEpithelial CellsHeat Shock Transcription FactorsHeat-Shock ProteinsIntracellular MembranesKidneyL-Lactate DehydrogenaseLLC-PK1 CellsMultienzyme ComplexesOctoxynolProteasome Endopeptidase ComplexSodium-Potassium-Exchanging ATPaseSolubilityStress, PhysiologicalSwineTranscription FactorsConceptsATP depletionRenal epitheliumLactate dehydrogenase releaseCellular ATPReduction of ATPRenal ischemiaIntracellular calciumActivation of HSF1Heat shock transcription factorDehydrogenase releaseControl ATPStress responseControl levelsProgressive accumulationProteasome inhibitionAdaptive inductionHSF activationRapid fallActivationEpitheliumIncremental increaseCellular disruptionResponseATPIschemia
1997
A Tyrosine-Based Signal Targets H/K-ATPase to a Regulated Compartment and Is Required for the Cessation of Gastric Acid Secretion
Courtois-Coutry N, Roush D, Rajendran V, McCarthy J, Geibel J, Kashgarian M, Caplan M. A Tyrosine-Based Signal Targets H/K-ATPase to a Regulated Compartment and Is Required for the Cessation of Gastric Acid Secretion. Cell 1997, 90: 501-510. PMID: 9267030, DOI: 10.1016/s0092-8674(00)80510-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalciumCOS CellsCytomegalovirusDNA PrimersEndocytosisGastric AcidGastric MucosaH(+)-K(+)-Exchanging ATPaseMacromolecular SubstancesMiceMice, TransgenicMicroscopy, ImmunoelectronMutagenesis, Site-DirectedParietal Cells, GastricPolymerase Chain ReactionPromoter Regions, GeneticRecombinant ProteinsSignal TransductionTransfectionTyrosineConceptsK-ATPase beta subunitTyrosine-based signalsK-ATPaseTyrosine-based endocytosis signalTyrosine residuesBeta subunitIntracellular storage compartmentEndocytosis signalCytoplasmic tailMutant betaRegulated compartmentsSecrete acidResidue sequenceStorage compartmentCell surfaceCell plasmalemmaSubunitsTransgenic miceParietal cellsGastric glandsCompartmentsSecretionAcid secretionReinternalizationPlasmalemma
1987
Parathyroid hormone directly inhibits tubular reabsorption of bicarbonate in normocalcaemic rats with chronic hyperparathyroidism
JAEGER P, JONES W, KASHGARIAN M, SEGRE G, HAYSLETT J. Parathyroid hormone directly inhibits tubular reabsorption of bicarbonate in normocalcaemic rats with chronic hyperparathyroidism. European Journal Of Clinical Investigation 1987, 17: 415-420. PMID: 3121345, DOI: 10.1111/j.1365-2362.1987.tb01136.x.Peer-Reviewed Original ResearchConceptsParathyroid hormonePTH infusionChronic hyperparathyroidismPlasma calciumAnimal modelsEffect of PTHProximal HCO3 reabsorptionChronic metabolic acidosisGroups of animalsPrimary hyperparathyroidismAlzet minipumpsSerum calciumTubular reabsorptionAcute studyMetabolic acidosisMetabolic alkalosisRenal handlingTubular acidificationAcid secretionGroup IIHCO3- reabsorptionFree dietHyperparathyroidismCa-free dietNormal levelsAnimal model of primary hyperparathyroidism
Jaeger P, Jones W, Kashgarian M, Baron R, Clemens T, Segre G, Hayslett J. Animal model of primary hyperparathyroidism. American Journal Of Physiology 1987, 252: e790-e798. PMID: 3591940, DOI: 10.1152/ajpendo.1987.252.6.e790.Peer-Reviewed Original ResearchConceptsTheoretical renal thresholdPrimary hyperparathyroidismPlasma levelsRenal thresholdAnimal modelsD plasma levelsPTH plasma levelsPlasma calcium levelsSynthetic parathyroid hormonePTH levelsDihydroxyvitamin DParathyroid hormoneParathyroidectomized animalsBovine PTHChronic hyperparathyroidismSustained elevationNormal limitsPlasma calciumHyperparathyroidismCalcium levelsOrgan systemsEpithelial functionControl valuesBasal levelsExperimental model
1986
Mechanism of Nephrocalcinosis in Primary Hyperparathyroidism
Jaeger P, Jones W, Hayslett J, Kashgarian M, Segre G. Mechanism of Nephrocalcinosis in Primary Hyperparathyroidism. Advances In Experimental Medicine And Biology 1986, 208: 379-382. PMID: 3565154, DOI: 10.1007/978-1-4684-5206-8_47.Peer-Reviewed Original Research
1969
Physiologic studies in renal osteodystrophy treated by subtotal parathyroidectomy
Gill G, Pallotta J, Kashgarian M, Kessner D, Epstein F. Physiologic studies in renal osteodystrophy treated by subtotal parathyroidectomy. The American Journal Of Medicine 1969, 46: 930-940. PMID: 5797916, DOI: 10.1016/0002-9343(69)90095-3.Peer-Reviewed Original ResearchConceptsSubtotal parathyroidectomyParathyroid hormoneRenal osteodystrophyAbnormal renal handlingAdvanced renal insufficiencyOsteitis fibrosa cysticaRenal tubular reabsorptionRoentgenologic evidenceRenal insufficiencyFibrosa cysticaPreoperative levelsMetastatic calcificationUremic patientsTubular reabsorptionParathyroid tissueMedullary cystsRenal handlingPhysiologic studiesPatientsParathyroidectomyBone healingHormoneOsteodystrophyHypercalciuriaCystica
1961
Renal Tubular Acidosis and Renal Potassium Wasting Acquired as a Result of Hypercalcemic Nephropathy
Ferris T, Kashgarian M, Levitin H, Brandt I, Epstein F. Renal Tubular Acidosis and Renal Potassium Wasting Acquired as a Result of Hypercalcemic Nephropathy. New England Journal Of Medicine 1961, 265: 924-928. PMID: 13892591, DOI: 10.1056/nejm196111092651902.Peer-Reviewed Original Research