2021
Podocyte Glucocorticoid Receptors Are Essential for Glomerular Endothelial Cell Homeostasis in Diabetes Mellitus
Srivastava SP, Zhou H, Setia O, Dardik A, Fernandez‐Hernando C, Goodwin J. Podocyte Glucocorticoid Receptors Are Essential for Glomerular Endothelial Cell Homeostasis in Diabetes Mellitus. Journal Of The American Heart Association 2021, 10: e019437. PMID: 34308664, PMCID: PMC8475689, DOI: 10.1161/jaha.120.019437.Peer-Reviewed Original ResearchConceptsDiabetic nephropathySegmental fibrosisFatty acid metabolismDiabetes mellitusEndothelial cellsPrimary podocytesReceptor knockout micePathogenesis of proteinuriaAdministration of streptozotocinProfibrotic gene expressionAcid metabolismGlomerular endothelial cellsSmooth muscle actinEndothelial cell homeostasisCarnitine palmitoyltransferase 1AFatty acid oxidationBackground ProteinuriaWorsened fibrosisClinical characteristicsFibrotic featuresGlomerular fibrosisGlomerular homeostasisPatient managementControl littermatesSevere disease
2018
Establishment of a Modified Collagen-Induced Arthritis Mouse Model to Investigate the Anti-inflammatory Activity of Progranulin in Inflammatory Arthritis
Wei J, Liu C. Establishment of a Modified Collagen-Induced Arthritis Mouse Model to Investigate the Anti-inflammatory Activity of Progranulin in Inflammatory Arthritis. Methods In Molecular Biology 2018, 1806: 305-313. PMID: 29956284, DOI: 10.1007/978-1-4939-8559-3_20.Peer-Reviewed Original ResearchConceptsChicken type II collagenArthritis mouse modelPGRN-deficient miceInflammatory arthritisAnti-inflammatory activityMouse modelDeficient miceCollagen-Induced Arthritis Mouse ModelProtective roleCollagen-induced arthritis (CIA) mouse modelAutoimmune inflammatory arthritisHuman rheumatoid arthritisAutoimmune modelComplete Freund'sRheumatoid arthritisDegenerative arthritisPathological featuresDegenerative osteoarthritisControl littermatesCIA modelArthritisHigh incidenceType II collagenProgranulinDisease models
2009
Deletion of the Met receptor in the collecting duct decreases renal repair following ureteral obstruction
Ma H, Saenko M, Opuko A, Togawa A, Soda K, Marlier A, Moeckel GW, Cantley LG, Ishibe S. Deletion of the Met receptor in the collecting duct decreases renal repair following ureteral obstruction. Kidney International 2009, 76: 868-876. PMID: 19675527, DOI: 10.1038/ki.2009.304.Peer-Reviewed Original ResearchConceptsUreteral obstructionFibrotic responseKnockout miceMet receptorAcute tubular necrosisPlasminogen activator inhibitor-1Unilateral ureteral obstructionTubular cell proliferationActivator inhibitor-1Conditional knockout miceHepatocyte growth factorKidney injuryRenal injuryTubular necrosisFunctional recoveryInterstitial fibrosisCre miceRenal repairNephron injuryControl littermatesObstructionGrowth factorMiceInhibitor-1Injury
2007
Loss of MMP-2 disrupts skeletal and craniofacial development and results in decreased bone mineralization, joint erosion and defects in osteoblast and osteoclast growth
Mosig RA, Dowling O, DiFeo A, Ramirez MC, Parker IC, Abe E, Diouri J, Al Aqeel AA, Wylie JD, Oblander SA, Madri J, Bianco P, Apte SS, Zaidi M, Doty SB, Majeska RJ, Schaffler MB, Martignetti JA. Loss of MMP-2 disrupts skeletal and craniofacial development and results in decreased bone mineralization, joint erosion and defects in osteoblast and osteoclast growth. Human Molecular Genetics 2007, 16: 1113-1123. PMID: 17400654, PMCID: PMC2576517, DOI: 10.1093/hmg/ddm060.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArthritisBone and BonesBone RemodelingCalcification, PhysiologicCell ProliferationCells, CulturedCraniofacial AbnormalitiesGene DeletionHumansImmunohistochemistryJointsMatrix Metalloproteinase 2MiceMice, KnockoutOsteoblastsOsteoclastsReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingTime FactorsTomography, X-Ray ComputedConceptsMMP2-/- miceMMP-2Arthritis syndromeArticular cartilage destructionOsteoclast growthBone mineral densityDays of lifeWeeks of lifeWeeks of ageMMP-2 overexpressionJoint erosionsBone lossCartilage destructionNormal cell numbersPathophysiological mechanismsOsteoclast numberVivo physiological roleMineral densityControl littermatesAnatomical distributionBone disordersMurine modelMineralization defectMulticentric osteolysisDisease pathogenesisEndothelial-Specific Expression of Mitochondrial Thioredoxin Improves Endothelial Cell Function and Reduces Atherosclerotic Lesions
Zhang H, Luo Y, Zhang W, He Y, Dai S, Zhang R, Huang Y, Bernatchez P, Giordano FJ, Shadel G, Sessa WC, Min W. Endothelial-Specific Expression of Mitochondrial Thioredoxin Improves Endothelial Cell Function and Reduces Atherosclerotic Lesions. American Journal Of Pathology 2007, 170: 1108-1120. PMID: 17322393, PMCID: PMC1864879, DOI: 10.2353/ajpath.2007.060960.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaApolipoproteins EAtherosclerosisCells, CulturedEndothelial CellsFlow CytometryImmunoblottingImmunohistochemistryMiceMice, TransgenicMicroscopy, ConfocalMitochondrial ProteinsNitric OxideReactive Oxygen SpeciesReverse Transcriptase Polymerase Chain ReactionThioredoxinsVasodilationConceptsTg miceAtherosclerotic lesionsOxidative stressNitric oxide levelsEC functionDeficient mouse modelEndothelial cell functionAtherosclerosis developmentEnhanced vasodilationVascular EC functionEndothelium functionApolipoprotein EControl littermatesMouse modelOxide levelsMice showCapacity of ECEndothelial-specific expressionEndothelial cellsCritical roleReactive oxygen speciesCell functionMiceTotal antioxidantsLesions
2005
The Cell-Surface Isoform of Colony Stimulating Factor 1 (CSF1) Restores but Does Not Completely Normalize Fecundity in CSF1-Deficient Mice1
Ovadia S, Insogna K, Yao GQ. The Cell-Surface Isoform of Colony Stimulating Factor 1 (CSF1) Restores but Does Not Completely Normalize Fecundity in CSF1-Deficient Mice1. Biology Of Reproduction 2005, 74: 331-336. PMID: 16237150, DOI: 10.1095/biolreprod.105.045047.Peer-Reviewed Original ResearchConceptsColony stimulating factor 1Viability of offspringReproductive defectsCell surfaceMembrane-bound isoformStimulating factor 1Cell surface isoformAlpha promoterMCSF1Transgenic animalsProteolytic sheddingCSF1 proteinMouse reproductionFactor 1ReproductionTransgenic male miceIsoformsTransgenic miceSperm numberOffspringTissue levelsMurine uterusGenetic absenceControl littermatesPromoterInsulin Receptor Substrate 2 Is Essential for Maturation and Survival of Photoreceptor Cells
Yi X, Schubert M, Peachey N, Suzuma K, Burks D, Kushner J, Suzuma I, Cahill C, Flint C, Dow M, Leshan R, King G, White M. Insulin Receptor Substrate 2 Is Essential for Maturation and Survival of Photoreceptor Cells. Journal Of Neuroscience 2005, 25: 1240-1248. PMID: 15689562, PMCID: PMC6725974, DOI: 10.1523/jneurosci.3664-04.2005.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnimalsAnimals, NewbornApoptosisCell SurvivalDiabetic RetinopathyEye ProteinsGene DeletionHomeodomain ProteinsHyperglycemiaHyperinsulinismInsulin Receptor Substrate ProteinsInsulin ResistanceInsulin-Like Growth Factor IIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutPhosphoproteinsPhosphorylationPhotic StimulationPhotoreceptor CellsProtein Processing, Post-TranslationalProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRetinal Ganglion CellsSignal TransductionTrans-ActivatorsConceptsIrs2-/- micePhotoreceptor cellsPlexiform layerInsulin receptor substrate 2Insulin receptor substrateInsulin-like growth factor 1 receptorGrowth factor 1 receptorMost photoreceptor cellsInner plexiform layerOuter plexiform layerFactor 1 receptorFinal common pathwaySurvival of photoreceptorsNormal electrical functionMonths of ageWeeks of ageReceptor substrateCellular growthSubstrate 2Akt phosphorylationGanglion cellsIRS2 expressionPharmacological strategiesControl littermatesPhotoreceptor degeneration
2003
The voltage-gated potassium channel Kv1.3 regulates energy homeostasis and body weight
Xu J, Koni PA, Wang P, Li G, Kaczmarek L, Wu Y, Li Y, Flavell RA, Desir GV. The voltage-gated potassium channel Kv1.3 regulates energy homeostasis and body weight. Human Molecular Genetics 2003, 12: 551-559. PMID: 12588802, DOI: 10.1093/hmg/ddg049.Peer-Reviewed Original ResearchConceptsBody weightBasal metabolic rateKv1.3 channelsDiet-induced obesityHigh-fat dietBody weight regulationT cell activationVoltage-gated potassium channel Kv1.3Voltage-gated potassium channelsPotassium channel Kv1.3Control littermatesFood intakeLittermate controlsKnockout miceWeight regulationIndirect calorimetryMetabolic rateChannel inhibitionCell activationEnergy homeostasisKnockout animalsPotassium channelsCell membrane potentialMiceChannel Kv1.3
2001
Analysis of SM22α-Deficient Mice Reveals Unanticipated Insights into Smooth Muscle Cell Differentiation and Function
Zhang J, Kim S, Helmke B, Yu W, Du K, Lu M, Strobeck M, Yu Q, Parmacek M. Analysis of SM22α-Deficient Mice Reveals Unanticipated Insights into Smooth Muscle Cell Differentiation and Function. Molecular And Cellular Biology 2001, 21: 1336-1344. PMID: 11158319, PMCID: PMC99586, DOI: 10.1128/mcb.2001.21.4.1336-1344.2001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationEmbryonic and Fetal DevelopmentGene Expression Regulation, DevelopmentalGene TargetingLac OperonMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicrofilament ProteinsMuscle DevelopmentMuscle ProteinsMuscle, SmoothSignal TransductionTranscriptional ActivationConceptsVisceral SMCsBacterial lacZ reporter geneLocal mesenchymeWestern blot analysisSmooth muscle cell differentiationBeta-galactosidase activityBlood pressureControl littermatesHeart ratePostnatal developmentHomeostatic functionsHistological analysisMiceContractile SMCsBlot analysisDorsal aortaLittermatesAngiogenic programMuscle cell differentiationSM22alphaYolk sacCephalic mesenchymeCell differentiationLacZ reporter geneDetectable beta-galactosidase activity
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply