2024
292-OR: Coenzyme A Synthase Knockdown Alleviates Metabolic Dysfunction–Associated Steatohepatitis via Decreasing Cholesterol in Liver Lipid Droplets
SAKUMA I, GASPAR R, NASIRI A, KAHN M, GUERRA M, YIMLAMAI D, MURRAY S, PERELIS M, BARNES W, VATNER D, PETERSEN K, SAMUEL V, SHULMAN G. 292-OR: Coenzyme A Synthase Knockdown Alleviates Metabolic Dysfunction–Associated Steatohepatitis via Decreasing Cholesterol in Liver Lipid Droplets. Diabetes 2024, 73 DOI: 10.2337/db24-292-or.Peer-Reviewed Original ResearchCholine-deficient l-amino acid-defined high-fat dietAccumulation of cholesterolMRNA expressionPlasma ALTL-amino acid-defined high-fat dietProtective effectLiver lipid dropletsType 2 diabetesPotential therapeutic approachHigh-fat dietDecreased plasma ALTFibrosis markersFree cholesterol accumulationLipid dropletsLiver inflammationDay 1Macrophage markersHepatic inflammationMouse modelMarker expressionTherapeutic approachesDay 2Day 3Day 7Fibrosis
2023
Immune dysfunction revealed by digital spatial profiling of immuno-oncology markers in progressive stages of renal cell carcinoma and in brain metastases
Schoenfeld D, Moutafi M, Martinez S, Djureinovic D, Merkin R, Adeniran A, Braun D, Signoretti S, Choueiri T, Parisi F, Hurwitz M, Rimm D, Wei W, Jilaveanu L, Kluger H. Immune dysfunction revealed by digital spatial profiling of immuno-oncology markers in progressive stages of renal cell carcinoma and in brain metastases. Journal For ImmunoTherapy Of Cancer 2023, 11: e007240. PMID: 37586773, PMCID: PMC10432651, DOI: 10.1136/jitc-2023-007240.Peer-Reviewed Original ResearchConceptsRenal cell carcinomaBrain metastasesPrimary tumorTumor microenvironmentDigital spatial profilingCell carcinomaActivation protein expressionInflammatory macrophage markersRCC brain metastasesInnate immune activatorsNormal kidney samplesProgressive stagesExtracranial metastasesTim-3Immune checkpointsImmune dysfunctionImmune activationRCC metastasisLonger survivalImmune activatorsMacrophage markersTreatment responseSeparate cohortTissue microarrayMetastatic samples
2021
Bone Marrow-Derived Progenitor Cells Contribute to Remodeling of the Postpartum Uterus
Tal R, Kisa J, Abuwala N, Kliman HJ, Shaikh S, Chen AY, Lyu F, Taylor HS. Bone Marrow-Derived Progenitor Cells Contribute to Remodeling of the Postpartum Uterus. Stem Cells 2021, 39: 1489-1505. PMID: 34224633, PMCID: PMC9313624, DOI: 10.1002/stem.3431.Peer-Reviewed Original ResearchConceptsPostpartum uterusEndometrial stem/progenitor cellsBone marrow-derived progenitor cellsMarrow-derived progenitor cellsF4/80 macrophage markerUterine tissue regenerationProgenitor cellsC57BL/6J female micePostpartum day 1Cytokeratin-positive epithelial cellsBlood vessel endotheliumStem/progenitor cellsPrepregnancy levelsBM transplantsEndometrial regenerationEndometrial cellsFemale miceMacrophage markersPan-leukocytesLuminal epitheliumBone marrowDay 1BMDCsUterine cellsVessel endothelium
2020
Chronic mTOR activation induces a degradative smooth muscle cell phenotype
Li G, Wang M, Caulk AW, Cilfone NA, Gujja S, Qin L, Chen PY, Chen Z, Yousef S, Jiao Y, He C, Jiang B, Korneva A, Bersi MR, Wang G, Liu X, Mehta S, Geirsson A, Gulcher JR, Chittenden TW, Simons M, Humphrey JD, Tellides G. Chronic mTOR activation induces a degradative smooth muscle cell phenotype. Journal Of Clinical Investigation 2020, 130: 1233-1251. PMID: 32039915, PMCID: PMC7269581, DOI: 10.1172/jci131048.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAortic Aneurysm, ThoracicAortic Dissectionbeta CateninDisease Models, AnimalLysosomesMechanistic Target of Rapamycin Complex 1MiceMice, Knockout, ApoEMicrophthalmia-Associated Transcription FactorMyocytes, Smooth MuscleSignal TransductionTOR Serine-Threonine KinasesTuberous Sclerosis Complex 1 ProteinConceptsMTOR activationMTOR complex 1Smooth muscle cell phenotypeMuscle cell phenotypeContext of hyperlipidemiaSmooth muscle cell proliferationThoracic aortic aneurysmDegradative organellesMuscle cell proliferationHematopoietic lineage markersSMC phenotypeLysosomal clearanceAdvanced diseaseMedial degenerationAortic diseaseLysosomal markersAortic aneurysmExtracellular matrixPhenotypic modulationConventional macrophagesMacrophage markersMedial SMCsConditional disruptionLineage markersImmune effectors
2018
CD68, CD163, and matrix metalloproteinase 9 (MMP-9) co-localization in breast tumor microenvironment predicts survival differently in ER-positive and -negative cancers
Pelekanou V, Villarroel-Espindola F, Schalper KA, Pusztai L, Rimm DL. CD68, CD163, and matrix metalloproteinase 9 (MMP-9) co-localization in breast tumor microenvironment predicts survival differently in ER-positive and -negative cancers. Breast Cancer Research 2018, 20: 154. PMID: 30558648, PMCID: PMC6298021, DOI: 10.1186/s13058-018-1076-x.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, CDAntigens, Differentiation, MyelomonocyticAntineoplastic AgentsBiomarkers, TumorBreastBreast NeoplasmsDisease-Free SurvivalFemaleGene Expression Regulation, NeoplasticHumansMacrophagesMatrix Metalloproteinase 9Middle AgedPatient SelectionPrognosisReceptors, Cell SurfaceReceptors, EstrogenRetrospective StudiesSurvival AnalysisTissue Array AnalysisTumor MicroenvironmentConceptsTumor-associated macrophagesOverall survivalQuantitative immunofluorescenceMacrophage markersBreast cancerHigh expressionPan-macrophage marker CD68Triple-negative breast cancerCD163/CD68Multiplexed quantitative immunofluorescenceImproved overall survivalProtein expressionWorse overall survivalPoor overall survivalMMP-9 protein expressionSubclass of patientsMacrophage-targeted therapiesMatrix metalloproteinase-9Tissue microarray formatMMP-9 proteinBreast tumor microenvironmentModulator of responseParaffin-embedded tissuesBreast cancer biomarkersCohort BImmunological differences between primary and metastatic breast cancer
Szekely B, Bossuyt V, Li X, Wali VB, Patwardhan GA, Frederick C, Silber A, Park T, Harigopal M, Pelekanou V, Zhang M, Yan Q, Rimm DL, Bianchini G, Hatzis C, Pusztai L. Immunological differences between primary and metastatic breast cancer. Annals Of Oncology 2018, 29: 2232-2239. PMID: 30203045, DOI: 10.1093/annonc/mdy399.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAntineoplastic Agents, ImmunologicalB7-H1 AntigenBiomarkers, TumorBiopsyBreast NeoplasmsDisease ProgressionDrug Resistance, NeoplasmFemaleGene Expression RegulationHumansImmunologic SurveillanceLymphocyte CountLymphocytes, Tumor-InfiltratingMiddle AgedMutation RateTumor EscapeTumor MicroenvironmentYoung AdultConceptsMetastatic breast cancerBreast cancerTherapeutic targetToll-like receptor pathway genesImmuno-oncology therapeutic targetsBreast cancer evolvesImmune proteasome expressionPD-L1 positivityCorresponding primary tumorsPotential therapeutic targetMHC class IImmune-related genesMetastatic cancer samplesLigand/receptor pairLymphocyte countT helperT-regsPD-L1Immune microenvironmentCytotoxic TPrimary tumorMastoid cellsDisease progressionTherapeutic combinationsMacrophage markers
2015
Protective role of G-CSF in dextran sulfate sodium-induced acute colitis through generating gut-homing macrophages
Meshkibaf S, Martins A, Henry G, Kim S. Protective role of G-CSF in dextran sulfate sodium-induced acute colitis through generating gut-homing macrophages. Cytokine 2015, 78: 69-78. PMID: 26687628, DOI: 10.1016/j.cyto.2015.11.025.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsCells, CulturedColitisDextran SulfateGranulocyte Colony-Stimulating FactorHomeostasisInterleukin-13Interleukin-1betaIntestinesLipopolysaccharidesMacrophage Colony-Stimulating FactorMacrophagesMiceNitric Oxide Synthase Type IIReceptors, Granulocyte Colony-Stimulating FactorTumor Necrosis Factor-alphaConceptsInducible nitric oxide synthaseBone marrow-derived macrophagesG-CSFMarrow-derived macrophagesColony-stimulating factorAcute colitisDextran sulfate sodium-induced acute colitisSeverity of colitisDextran sulfate sodiumReceptor-deficient miceGranulocyte colony-stimulating factorDeath ligand 2Function of neutrophilsNitric oxide synthaseTumor necrosis factorMacrophage colony-stimulating factorRegulatory macrophage markersAdoptive transferSulfate sodiumIL-1βImmune homeostasisOxide synthaseMacrophage markersNecrosis factorImmune regulation
2005
Expression of Mediators of Renal Injury in the Remnant Kidney of ROP Mice Is Attenuated by Cyclooxygenase-2 Inhibition
Cheng H, Zhang M, Moeckel GW, Zhao Y, Wang S, Qi Z, Breyer MD, Harris RC. Expression of Mediators of Renal Injury in the Remnant Kidney of ROP Mice Is Attenuated by Cyclooxygenase-2 Inhibition. Nephron 2005, 101: e75-e85. PMID: 15995341, DOI: 10.1159/000086645.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsConnective Tissue Growth FactorCyclooxygenase 2 InhibitorsFibronectinsGlomerulosclerosis, Focal SegmentalImmediate-Early ProteinsIntercellular Signaling Peptides and ProteinsKidneyKidney TubulesMiceMice, Inbred StrainsNephrectomyProteinuriaProto-Oncogene Proteins c-metPyrazolesSulfonamidesTissue DistributionConceptsCyclooxygenase-2 inhibitionROP miceSC58236 treatmentRenal injuryRemnant kidneyImmunoreactive COX-2Immunoreactive TGF-beta1Selective COX-2 inhibitorsSystemic blood pressureConnective tissue growth factorSubtotal renal ablationRenal tubulointerstitial injuryExpression of mediatorsCOX-2 inhibitorsTissue growth factorCollagen IV mRNATubulointerstitial injuryBlood pressureRenal ablationSignificant albuminuriaCOX-2Macrophage markersMouse modelTGF-beta1Remnant group
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