2021
MicroRNA miR-24-3p reduces DNA damage responses, apoptosis, and susceptibility to chronic obstructive pulmonary disease
Nouws J, Wan F, Finnemore E, Roque W, Kim SJ, Bazan IS, Li CX, Sköld C, Dai Q, Yan X, Chioccioli M, Neumeister V, Britto CJ, Sweasy J, Bindra RS, Wheelock ÅM, Gomez JL, Kaminski N, Lee PJ, Sauler M. MicroRNA miR-24-3p reduces DNA damage responses, apoptosis, and susceptibility to chronic obstructive pulmonary disease. JCI Insight 2021, 6: e134218. PMID: 33290275, PMCID: PMC7934877, DOI: 10.1172/jci.insight.134218.Peer-Reviewed Original ResearchConceptsCellular stress responseStress responseHomology-directed DNA repairDNA damage responseProtein BRCA1Damage responseCellular stressDNA repairProtein BimCOPD lung tissueLung epithelial cellsCellular responsesExpression arraysEpithelial cell apoptosisDNA damageChronic obstructive pulmonary diseaseBRCA1 expressionCell apoptosisApoptosisEpithelial cellsCritical mechanismMicroRNAsRegulatorObstructive pulmonary diseaseIncreases Susceptibility
2018
Chapter 9 Medical Aspects of the Treatment of Lower Urinary Tract Symptoms/Benign Prostatic Hyperplasia: 5-Alpha Reductase Inhibitors
Cavallo J, Kaplan S. Chapter 9 Medical Aspects of the Treatment of Lower Urinary Tract Symptoms/Benign Prostatic Hyperplasia: 5-Alpha Reductase Inhibitors. 2018, 189-206. DOI: 10.1016/b978-0-12-811397-4.00009-3.Peer-Reviewed Original ResearchMaximum urinary flow rateInitial prostate volumeAcute urinary retentionUrinary flow rateProstate volumeUrinary retentionClinical progressionSymptom scoresLower Urinary Tract Symptoms/Benign Prostatic HyperplasiaUrinary tract symptoms/benign prostatic hyperplasiaAlpha-1 adrenergic receptor blockerLower urinary tract symptomsReductase inhibitorsAlpha-1 adrenergic receptorsSpecific antigen valuesPostvoid residual volumeSexual side effectsUrinary tract symptomsAdrenergic receptor blockersBenign prostatic hyperplasiaLong-term treatmentConversion of testosteroneHigher initial PSAEpithelial cell apoptosisReceptor blockers
2016
Mice lacking myosin IXb, an inflammatory bowel disease susceptibility gene, have impaired intestinal barrier function and superficial ulceration in the ileum
Hegan PS, Chandhoke SK, Barone C, Egan M, Bähler M, Mooseker MS. Mice lacking myosin IXb, an inflammatory bowel disease susceptibility gene, have impaired intestinal barrier function and superficial ulceration in the ileum. Cytoskeleton 2016, 73: 163-179. PMID: 26972322, DOI: 10.1002/cm.21292.Peer-Reviewed Original ResearchConceptsInflammatory bowel diseaseIntestinal barrier functionBarrier functionSuperficial ulcerationKO miceFeatures of IBDDextran sulfate sodium-induced colitisIntestinal mucosal damageMucosal barrier functionSodium-induced colitisFecal occult bloodIntestinal epithelial cell apoptosisInflammatory bowel disease susceptibility genesEpithelial cell apoptosisSusceptibility genesMyosin IXbTransepithelial electrical resistanceNeutrophil infiltrationMucosal damageBowel diseaseOccult bloodSurface ulcerationDisease onsetIntestinal mucosaFocal lesions
2014
Hepatocyte Growth Factor (Hgf) Stimulates Low Density Lipoprotein Receptor-related Protein (Lrp) 5/6 Phosphorylation and Promotes Canonical Wnt Signaling*
Koraishy FM, Silva C, Mason S, Wu D, Cantley LG. Hepatocyte Growth Factor (Hgf) Stimulates Low Density Lipoprotein Receptor-related Protein (Lrp) 5/6 Phosphorylation and Promotes Canonical Wnt Signaling*. Journal Of Biological Chemistry 2014, 289: 14341-14350. PMID: 24692544, PMCID: PMC4022900, DOI: 10.1074/jbc.m114.563213.Peer-Reviewed Original ResearchConceptsΒ-catenin stabilizationRenal ischemic injuryLRP5/6 phosphorylationEpithelial cell responsesRenal proximal tubulesEpithelial cell apoptosisHepatocyte growth factorCanonical WntActive GSK3Ischemic injuryRenal epithelial cellsProximal tubulesCell responsesCanonical Wnt signalingHGF treatmentGrowth factorCell apoptosisEpithelial cellsHGFMet receptorImportant transactivatorWnt signalingInjuryLRP5/6MetS
2013
Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling
Shi Y, Gochuico BR, Yu G, Tang X, Osorio JC, Fernandez IE, Risquez CF, Patel AS, Shi Y, Wathelet MG, Goodwin AJ, Haspel JA, Ryter SW, Billings EM, Kaminski N, Morse D, Rosas IO. Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling. American Journal Of Respiratory And Critical Care Medicine 2013, 188: 831-841. PMID: 23924348, PMCID: PMC3826270, DOI: 10.1164/rccm.201303-0434oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBleomycinBronchoalveolar LavageCaveolin 1Disease Models, AnimalGene Expression ProfilingGenetic MarkersHumansHydroxyprolineIdiopathic Pulmonary FibrosisIn Vitro TechniquesMacrophages, AlveolarMiceMice, TransgenicSignal TransductionSyndecan-2Tissue Array AnalysisTransforming Growth Factor beta1Up-RegulationConceptsHuman syndecan-2TGF-β1 target genesSyndecan-2Target genesIdiopathic pulmonary fibrosisEpithelial cell apoptosisAlveolar epithelial cellsEpithelial cellsTransforming Growth Factor-β1 SignalingCell apoptosisAntifibrotic effectsTGF-β1TGF-β signalingLung injuryPulmonary fibrosisAlveolar epithelial cell apoptosisExtracellular matrix productionTransgenic miceGrowth factor-β1 (TGF-β1) signalingMacrophage-specific overexpressionLung fibrosisMicroarray assayΒ1 signalingAlveolar macrophagesDownstream expression
2010
Role of Breast Regression Protein–39 in the Pathogenesis of Cigarette Smoke–Induced Inflammation and Emphysema
Matsuura H, Hartl D, Kang MJ, Dela Cruz CS, Koller B, Chupp GL, Homer RJ, Zhou Y, Cho WK, Elias JA, Lee CG. Role of Breast Regression Protein–39 in the Pathogenesis of Cigarette Smoke–Induced Inflammation and Emphysema. American Journal Of Respiratory Cell And Molecular Biology 2010, 44: 777-786. PMID: 20656949, PMCID: PMC3135840, DOI: 10.1165/rcmb.2010-0081oc.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseBRP-39/YKLBreast regression protein 39YKL-40BRP-39Alveolar destructionCigarette smokeChitinase-like protein YKL-40Emphysematous alveolar destructionLungs of CSObstructive pulmonary diseaseProtein YKL-40Excessive inflammatory responseAirway epithelial cellsAlveolar type II cellsNull mutant miceProtein 39Epithelial cell apoptosisType II cellsCurrent smokersPulmonary diseaseBronchoalveolar lavageTissue inflammationEmphysematous destructionSerum concentrationsPMCA2 regulates apoptosis during mammary gland involution and predicts outcome in breast cancer
VanHouten J, Sullivan C, Bazinet C, Ryoo T, Camp R, Rimm DL, Chung G, Wysolmerski J. PMCA2 regulates apoptosis during mammary gland involution and predicts outcome in breast cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 11405-11410. PMID: 20534448, PMCID: PMC2895115, DOI: 10.1073/pnas.0911186107.Peer-Reviewed Original ResearchConceptsPMCA2 expressionBreast cancerT47D breast cancer cellsIntracellular calcium levelsBreast cancer progressionBreast cancer cellsEpithelial cell apoptosisPoor outcomeIntracellular calciumCalcium levelsMammary gland involutionCancer progressionCell apoptosisCancer cellsMammary involutionApoptosisGland involutionCancerMammary epithelial cell apoptosisOutcomesPMCA2Triggers apoptosisApical surfaceExpressionOverexpression
2009
Acidic Mammalian Chitinase Regulates Epithelial Cell Apoptosis via a Chitinolytic-Independent Mechanism
Hartl D, He CH, Koller B, Da Silva CA, Kobayashi Y, Lee CG, Flavell RA, Elias JA. Acidic Mammalian Chitinase Regulates Epithelial Cell Apoptosis via a Chitinolytic-Independent Mechanism. The Journal Of Immunology 2009, 182: 5098-5106. PMID: 19342690, PMCID: PMC2666938, DOI: 10.4049/jimmunol.0803446.Peer-Reviewed Original ResearchConceptsAcidic mammalian chitinaseTh2-mediated diseasesEpithelial cellsMammalian chitinasePI3K/Akt pathwayPulmonary epithelial cellsEpithelial cell apoptosisApoptosis-inhibiting effectsComparable cytoprotectionGrowth factor withdrawal-induced apoptosisChitinolytic activityEffector responsesParacrine mannerFas ligand-induced apoptosisAntiparasite responsesGrowth factor withdrawalWithdrawal-induced apoptosisLigand-induced apoptosisFas ligandAkt pathwayCell apoptosisAkt phosphorylationAMCaseBiologic propertiesCytoprotection
2005
Regulation of lung injury and repair by Toll-like receptors and hyaluronan
Jiang D, Liang J, Fan J, Yu S, Chen S, Luo Y, Prestwich GD, Mascarenhas MM, Garg HG, Quinn DA, Homer RJ, Goldstein DR, Bucala R, Lee PJ, Medzhitov R, Noble PW. Regulation of lung injury and repair by Toll-like receptors and hyaluronan. Nature Medicine 2005, 11: 1173-1179. PMID: 16244651, DOI: 10.1038/nm1315.Peer-Reviewed Original ResearchConceptsAcute lung injuryLung injuryToll-like receptorsInflammatory responseTLR2-dependent mannerSera of individualsCell-specific overexpressionEpithelial cell apoptosisEpithelial cell integrityHyaluronan degradation productsChemokine productionInflammatory cellsTissue injuryExtracellular matrix glycosaminoglycan hyaluronanTransepithelial migrationInjuryCell surface hyaluronanHyaluronan fragmentsCell apoptosisBasal activationClearance resultsInflammationGlycosaminoglycan hyaluronanReceptorsHyaluronanRole of cathepsin S-dependent epithelial cell apoptosis in IFN-γ-induced alveolar remodeling and pulmonary emphysema
Zheng T, Kang M, Crothers K, Zhu Z, Liu W, Lee C, Rabach L, Chapman H, Homer R, Aldous D, DeSanctis G, Underwood S, Graupe M, Flavell R, Schmidt J, Elias J. Role of cathepsin S-dependent epithelial cell apoptosis in IFN-γ-induced alveolar remodeling and pulmonary emphysema. The Journal Of Immunology 2005, 175: 2026-2026. DOI: 10.4049/jimmunol.175.3.2026-a.Peer-Reviewed Original ResearchEpithelial cell apoptosisRole of Cathepsin S-Dependent Epithelial Cell Apoptosis in IFN-γ-Induced Alveolar Remodeling and Pulmonary Emphysema
Zheng T, Kang MJ, Crothers K, Zhu Z, Liu W, Lee CG, Rabach LA, Chapman HA, Homer RJ, Aldous D, DeSanctis G, Underwood S, Graupe M, Flavell RA, Schmidt JA, Elias JA. Role of Cathepsin S-Dependent Epithelial Cell Apoptosis in IFN-γ-Induced Alveolar Remodeling and Pulmonary Emphysema. The Journal Of Immunology 2005, 174: 8106-8115. PMID: 15944319, DOI: 10.4049/jimmunol.174.12.8106.Peer-Reviewed Original ResearchConceptsNull mutationEpithelial cell apoptosisCell apoptosisDNA injuryTissue remodelingProtease accumulationCaspase inhibitorsMitochondrial apoptosis pathway activationDeath receptorsPropidium iodide stainingCathepsin SHuman diseasesApoptosis responseApoptosis pathway activationApoptosis inhibitionCaspase-3ApoptosisIodide stainingPathway activationCathepsin S inhibitionMutationsRemodelingCritical eventsAlveolar remodelingIFN-gammaBcl-2–related protein A1 is an endogenous and cytokine-stimulated mediator of cytoprotection in hyperoxic acute lung injury
He CH, Waxman AB, Lee CG, Link H, Rabach ME, Ma B, Chen Q, Zhu Z, Zhong M, Nakayama K, Nakayama KI, Homer R, Elias JA. Bcl-2–related protein A1 is an endogenous and cytokine-stimulated mediator of cytoprotection in hyperoxic acute lung injury. Journal Of Clinical Investigation 2005, 115: 1039-1048. PMID: 15841185, PMCID: PMC1070412, DOI: 10.1172/jci23004.Peer-Reviewed Original ResearchConceptsHyperoxic acute lung injuryAcute lung injuryLung injuryIL-11Bcl-2Alveolar protein leakBcl-xLToxic effectsEpithelial cell apoptosisWT miceProtein leakMurine survivalExpression of A1Survival advantageBfl-1/A1Protective responsePremature deathHyperoxiaA1 overexpressionBcl-2 proteinMiceCell apoptosisCritical mediatorInjuryNecrosis
2001
Temporally regulated overexpression of parathyroid hormone-related protein in the mammary gland reveals distinct fetal and pubertal phenotypes
Dunbar ME, Dann P, Brown CW, Van Houton J, Dreyer B, Philbrick WP, Wysolmerski JJ. Temporally regulated overexpression of parathyroid hormone-related protein in the mammary gland reveals distinct fetal and pubertal phenotypes. Journal Of Endocrinology 2001, 171: 403-416. PMID: 11739006, DOI: 10.1677/joe.0.1710403.Peer-Reviewed Original ResearchConceptsParathyroid hormone-related proteinHormone-related proteinPTHrP overexpressionMammary glandLobuloalveolar developmentDuctal elongationMammary developmentOverexpression of PTHrPDouble transgenic miceTransgenic mice resultsTerminal end budsEpithelial cell apoptosisPubertal phenotypesDuctal branchingEmbryonic mammary developmentTransgenic miceMice resultsPTHrPEnd budsDecrease apoptosisCell apoptosisBasal rateDuctal morphogenesisCell proliferationDuctal tree
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