2024
Fatty acid binding protein 5 suppression attenuates obesity-induced hepatocellular carcinoma by promoting ferroptosis and intratumoral immune rewiring
Sun J, Esplugues E, Bort A, Cardelo M, Ruz-Maldonado I, Fernández-Tussy P, Wong C, Wang H, Ojima I, Kaczocha M, Perry R, Suárez Y, Fernández-Hernando C. Fatty acid binding protein 5 suppression attenuates obesity-induced hepatocellular carcinoma by promoting ferroptosis and intratumoral immune rewiring. Nature Metabolism 2024, 6: 741-763. PMID: 38664583, DOI: 10.1038/s42255-024-01019-6.Peer-Reviewed Original ResearchConceptsFatty acid binding protein 5Tumor-associated macrophagesHepatocellular carcinomaImmunosuppressive phenotype of tumor-associated macrophagesIncreased CD8+ T cell activationCD8+ T cell activationPhenotype of tumor-associated macrophagesPro-inflammatory tumor microenvironmentCo-stimulatory molecules CD80T cell activationHepatocellular carcinoma burdenTransformation of hepatocytesBinding protein 5Potential therapeutic approachImmunosuppressive phenotypeTumor microenvironmentFerroptosis-induced cell deathMale miceEnhanced ferroptosisTherapeutic approachesPharmacological inhibitionGenetic ablationIncreased expressionSingle-cell atlasAnalysis of transformed cells
2021
MMAB promotes negative feedback control of cholesterol homeostasis
Goedeke L, Canfrán-Duque A, Rotllan N, Chaube B, Thompson BM, Lee RG, Cline GW, McDonald JG, Shulman GI, Lasunción MA, Suárez Y, Fernández-Hernando C. MMAB promotes negative feedback control of cholesterol homeostasis. Nature Communications 2021, 12: 6448. PMID: 34750386, PMCID: PMC8575900, DOI: 10.1038/s41467-021-26787-7.Peer-Reviewed Original ResearchMeSH KeywordsAlkyl and Aryl TransferasesAnimalsCell Line, TumorCholesterolCholesterol, LDLFeedback, PhysiologicalGene Expression ProfilingHeLa CellsHep G2 CellsHomeostasisHumansHydroxymethylglutaryl CoA ReductasesLiverMice, Inbred C57BLMice, KnockoutPromoter Regions, GeneticReceptors, LDLRNA InterferenceSterol Regulatory Element Binding Protein 2ConceptsCholesterol biosynthesisCholesterol homeostasisMouse hepatic cell lineIntegrative genomic strategyIntricate regulatory networkMaster transcriptional regulatorCellular cholesterol levelsHMGCR activityLDL-cholesterol uptakeCholesterol levelsHuman hepatic cellsSterol contentGenomic strategiesTranscriptional regulatorsRegulatory networksIntracellular cholesterol levelsGene expressionUnexpected roleHepatic cell linesBiosynthesisMMABIntracellular levelsCell linesHomeostasisExpression of SREBP2Ketogenic diet restrains aging-induced exacerbation of coronavirus infection in mice
Ryu S, Shchukina I, Youm YH, Qing H, Hilliard B, Dlugos T, Zhang X, Yasumoto Y, Booth CJ, Fernández-Hernando C, Suárez Y, Khanna K, Horvath TL, Dietrich MO, Artyomov M, Wang A, Dixit VD. Ketogenic diet restrains aging-induced exacerbation of coronavirus infection in mice. ELife 2021, 10: e66522. PMID: 34151773, PMCID: PMC8245129, DOI: 10.7554/elife.66522.Peer-Reviewed Original ResearchConceptsΓδ T cellsKetogenic dietCoronavirus infectionAged miceT cellsHigher systemic inflammationInfected aged miceCOVID-19 severityCOVID-19 infectionActivation of ketogenesisMouse hepatitis virus strain A59Systemic inflammationInflammatory damageInfluenza infectionClinical hallmarkNLRP3 inflammasomeImmune surveillanceAdipose tissuePotential treatmentInfectionMiceStrongest predictorLungMortalityAgeGene Expression Signature in Patients With Symptomatic Peripheral Artery Disease
Newman JD, Cornwell MG, Zhou H, Rockman C, Heguy A, Suarez Y, Cheng HS, Feinberg MW, Hochman JS, Ruggles KV, Berger JS. Gene Expression Signature in Patients With Symptomatic Peripheral Artery Disease. Arteriosclerosis Thrombosis And Vascular Biology 2021, 41: 1521-1533. PMID: 33657880, PMCID: PMC8048111, DOI: 10.1161/atvbaha.120.315857.Peer-Reviewed Original Research
2020
Cav-1 (Caveolin-1) Deficiency Increases Autophagy in the Endothelium and Attenuates Vascular Inflammation and Atherosclerosis
Zhang X, Ramírez CM, Aryal B, Madrigal-Matute J, Liu X, Diaz A, Torrecilla-Parra M, Suárez Y, Cuervo AM, Sessa WC, Fernández-Hernando C. Cav-1 (Caveolin-1) Deficiency Increases Autophagy in the Endothelium and Attenuates Vascular Inflammation and Atherosclerosis. Arteriosclerosis Thrombosis And Vascular Biology 2020, 40: 1510-1522. PMID: 32349535, PMCID: PMC7253189, DOI: 10.1161/atvbaha.120.314291.Peer-Reviewed Original ResearchConceptsCav-1 deficiencyCav-1-deficient miceCav-1Autophagic fluxCholesterol-rich membrane domainsCav-1 interactsATG5-ATG12 complexEndothelial Cav-1 expressionRegulation of autophagyNovel molecular mechanismExtracellular matrix remodelingAutophagosome componentsMembrane domainsLipid raftsAutophagosome formationPlasma membraneCav-1 expressionMolecular mechanismsLDL transcytosisCellular localizationImportant regulatorAutophagyAutophagy contributesRelevant regulatorMatrix remodeling
2019
Genetic deficiency or pharmacological inhibition of miR-33 protects from kidney fibrosis
Price NL, Miguel V, Ding W, Singh AK, Malik S, Rotllan N, Moshnikova A, Toczek J, Zeiss C, Sadeghi MM, Arias N, Baldán Á, Andreev OA, Rodríguez-Puyol D, Bahal R, Reshetnyak YK, Suárez Y, Fernández-Hernando C, Lamas S. Genetic deficiency or pharmacological inhibition of miR-33 protects from kidney fibrosis. JCI Insight 2019, 4 PMID: 31613798, PMCID: PMC6948871, DOI: 10.1172/jci.insight.131102.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsFatty AcidsFibrosisKidney DiseasesMaleMiceMice, Inbred C57BLMice, KnockoutMicroRNAsOxidation-ReductionConceptsFatty acid oxidationChronic kidney diseaseKidney diseaseDisease progressionMiR-33Bone marrow transplantExtent of fibrosisDevelopment of fibrosisAttractive therapeutic targetExpression of factorsNucleic acid inhibitorsMarrow transplantKidney fibrosisFibrotic kidneysMouse modelTherapeutic targetLipid metabolismPharmacological inhibitionFibrosisLipid accumulationDiseaseGenetic deficiencyProgressionKidneyAcid oxidationSuppressing miR-21 activity in tumor-associated macrophages promotes an antitumor immune response
Sahraei M, Chaube B, Liu Y, Sun J, Kaplan A, Price NL, Ding W, Oyaghire S, García-Milian R, Mehta S, Reshetnyak YK, Bahal R, Fiorina P, Glazer PM, Rimm DL, Fernández-Hernando C, Suárez Y. Suppressing miR-21 activity in tumor-associated macrophages promotes an antitumor immune response. Journal Of Clinical Investigation 2019, 129: 5518-5536. PMID: 31710308, PMCID: PMC6877327, DOI: 10.1172/jci127125.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChemokine CXCL10Cytotoxicity, ImmunologicInterleukin-12MacrophagesMiceMice, Inbred C57BLMicroRNAsNeoplasmsTumor MicroenvironmentConceptsTumor-associated macrophagesMiR-21 expressionTumor growthMiR-21Immune responseCytotoxic T cell responsesC motif chemokine 10Antitumor immune responseT cell responsesAntitumoral immune responseTumor immune infiltratesInduction of cytokinesPotential therapeutic implicationsMiR-21 inhibitionStages of carcinogenesisAngiostatic phenotypeTumor cell deathIL-12Immune infiltratesTherapeutic implicationsSolid tumorsTumor neovascularizationTumor progressionTumor microenvironmentTumor pathogenesisCaveolin-1 Regulates Atherogenesis by Attenuating Low-Density Lipoprotein Transcytosis and Vascular Inflammation Independently of Endothelial Nitric Oxide Synthase Activation
Ramírez CM, Zhang X, Bandyopadhyay C, Rotllan N, Sugiyama MG, Aryal B, Liu X, He S, Kraehling JR, Ulrich V, Lin CS, Velazquez H, Lasunción MA, Li G, Suárez Y, Tellides G, Swirski FK, Lee WL, Schwartz MA, Sessa WC, Fernández-Hernando C. Caveolin-1 Regulates Atherogenesis by Attenuating Low-Density Lipoprotein Transcytosis and Vascular Inflammation Independently of Endothelial Nitric Oxide Synthase Activation. Circulation 2019, 140: 225-239. PMID: 31154825, PMCID: PMC6778687, DOI: 10.1161/circulationaha.118.038571.Peer-Reviewed Original ResearchConceptsEndothelial nitric oxide synthaseDiet-induced atherosclerosisNO productionVascular inflammationENOS activationEndothelial nitric oxide synthase activationNitric oxide synthase activationAthero-protective functionsLipid metabolic factorsEndothelial cell inflammationNitric oxide synthaseWild-type miceMice Lacking ExpressionProduction of NOExtracellular matrix remodelingInflammatory primingHyperlipidemic miceInflammatory pathwaysAortic archCell inflammationOxide synthaseMetabolic factorsMouse modelAtherosclerosisInflammation
2018
Inhibition of profibrotic microRNA-21 affects platelets and their releasate
Barwari T, Eminaga S, Mayr U, Lu R, Armstrong PC, Chan MV, Sahraei M, Fernández-Fuertes M, Moreau T, Barallobre-Barreiro J, Lynch M, Yin X, Schulte C, Baig F, Pechlaner R, Langley SR, Zampetaki A, Santer P, Weger M, Plasenzotti R, Schosserer M, Grillari J, Kiechl S, Willeit J, Shah AM, Ghevaert C, Warner TD, Fernández-Hernando C, Suárez Y, Mayr M. Inhibition of profibrotic microRNA-21 affects platelets and their releasate. JCI Insight 2018, 3: e123335. PMID: 30385722, PMCID: PMC6238735, DOI: 10.1172/jci.insight.123335.Peer-Reviewed Original ResearchConceptsMiR-21 inhibitionMiR-21TGF-β1TGF-β1 secretionMiR-21 levelsMiR-21 mimicsMiR-21 inhibitorMurine cardiac fibroblastsBruneck StudyLow plateletsAntifibrotic effectsProfibrotic factorsLeukocyte countSpecific therapyClinical trialsOrgan diseaseTGF-β1 releaseLittermate controlsBone marrowCardiac fibroblastsMegakaryocyte numberMouse heartsFibrosisPlasma samplesPlatelet releaseBrown adipose tissue derived ANGPTL4 controls glucose and lipid metabolism and regulates thermogenesis
Singh AK, Aryal B, Chaube B, Rotllan N, Varela L, Horvath TL, Suárez Y, Fernández-Hernando C. Brown adipose tissue derived ANGPTL4 controls glucose and lipid metabolism and regulates thermogenesis. Molecular Metabolism 2018, 11: 59-69. PMID: 29627378, PMCID: PMC6001401, DOI: 10.1016/j.molmet.2018.03.011.Peer-Reviewed Original ResearchConceptsBrown adipose tissueAdipose tissueAbsence of ANGPTL4Lipoprotein metabolismLPL activityShort-term HFD feedingTriglyceride-rich lipoprotein catabolismLipoprotein lipaseRole of ANGPTL4Novel mouse modelAcute cold exposureGlucose toleranceHFD feedingFatty acidsLipoprotein catabolismWhole body lipidGlucose homeostasisMouse modelGlucose metabolismTAG clearanceBAT resultsLipid metabolismANGPTL4Cold exposureFA oxidationAbsence of ANGPTL4 in adipose tissue improves glucose tolerance and attenuates atherogenesis
Aryal B, Singh AK, Zhang X, Varela L, Rotllan N, Goedeke L, Chaube B, Camporez JP, Vatner DF, Horvath TL, Shulman GI, Suárez Y, Fernández-Hernando C. Absence of ANGPTL4 in adipose tissue improves glucose tolerance and attenuates atherogenesis. JCI Insight 2018, 3: e97918. PMID: 29563332, PMCID: PMC5926923, DOI: 10.1172/jci.insight.97918.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAdipose TissueAllelesAngiopoietin-Like Protein 4AnimalsAtherosclerosisBody WeightChemokinesCytokinesDiet, High-FatDiet, WesternFatty AcidsGene Expression ProfilingGene Expression RegulationGene Knockout TechniquesGlucoseInsulinIntegrasesIntercellular Signaling Peptides and ProteinsLipid MetabolismLipoprotein LipaseLipoproteinsLiverMaleMiceMice, Inbred C57BLMice, KnockoutMusclesObesityProprotein Convertase 9TriglyceridesConceptsAngiopoietin-like protein 4High-fat dietEctopic lipid depositionLipid depositionGlucose toleranceLipoprotein lipaseShort-term high-fat dietSevere metabolic abnormalitiesProgression of atherosclerosisMajor risk factorTriacylglycerol-rich lipoproteinsFatty acid uptakeAdipose tissue resultsProatherogenic lipoproteinsCardiometabolic diseasesMetabolic abnormalitiesKO miceRisk factorsWhole body lipidMetabolic disordersGlucose metabolismLPL activityAdipose tissueGenetic ablationRapid clearanceGenetic Ablation of miR-33 Increases Food Intake, Enhances Adipose Tissue Expansion, and Promotes Obesity and Insulin Resistance
Price NL, Singh AK, Rotllan N, Goedeke L, Wing A, Canfrán-Duque A, Diaz-Ruiz A, Araldi E, Baldán Á, Camporez JP, Suárez Y, Rodeheffer MS, Shulman GI, de Cabo R, Fernández-Hernando C. Genetic Ablation of miR-33 Increases Food Intake, Enhances Adipose Tissue Expansion, and Promotes Obesity and Insulin Resistance. Cell Reports 2018, 22: 2133-2145. PMID: 29466739, PMCID: PMC5860817, DOI: 10.1016/j.celrep.2018.01.074.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAdiposityAnimalsCholesterol, HDLCholesterol, LDLEatingEnzyme ActivationGene DeletionGene Expression RegulationGenetic Predisposition to DiseaseGerm CellsInflammation MediatorsInsulin ResistanceLipid MetabolismLiverMice, Inbred C57BLMicroRNAsModels, BiologicalObesityProtein Kinase C-epsilonSterol Regulatory Element Binding Protein 1ConceptsMiR-33Insulin resistanceFood intakeIncreases food intakeAdipose tissue expansionKey metabolic tissuesWild-type animalsPromotes obesityImpaired lipolysisPair feedingCardiovascular diseaseMetabolic dysfunctionTherapeutic modulationAdipose tissueLipid uptakeMiRNA-based therapiesMetabolic tissuesGenetic ablationTissue expansionMiceObesityTherapyDeleterious effectsDiseasePrevious reports
2017
Genetic Dissection of the Impact of miR-33a and miR-33b during the Progression of Atherosclerosis
Price NL, Rotllan N, Canfrán-Duque A, Zhang X, Pati P, Arias N, Moen J, Mayr M, Ford DA, Baldán Á, Suárez Y, Fernández-Hernando C. Genetic Dissection of the Impact of miR-33a and miR-33b during the Progression of Atherosclerosis. Cell Reports 2017, 21: 1317-1330. PMID: 29091769, PMCID: PMC5687841, DOI: 10.1016/j.celrep.2017.10.023.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAtherosclerosisATP Binding Cassette Transporter 1Blood GlucoseCells, CulturedCholesterolCholesterol, HDLDisease ProgressionGene Regulatory NetworksMacrophages, PeritonealMaleMiceMice, Inbred C57BLMice, KnockoutMicroRNAsMitochondrial Trifunctional Protein, beta SubunitMyocardiumReceptors, LDLConceptsPlaque burdenMiR-33MiR-33-deficient miceReduced plaque burdenProgression of atherosclerosisPro-atherogenic effectsMacrophage cholesterol effluxDecreases lipid accumulationTreatment of atherosclerosisMacrophage-specific lossMiR-33 deficiencyPromotes obesityHDL levelsInsulin resistancePlaque macrophagesProtective effectHyperlipidemic conditionsCholesterol effluxPlaque developmentLipid metabolismAtherosclerosisLipid accumulationHDL biogenesisPromising targetMacrophagesMacrophage deficiency of miR‐21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis
Canfrán‐Duque A, Rotllan N, Zhang X, Fernández‐Fuertes M, Ramírez‐Hidalgo C, Araldi E, Daimiel L, Busto R, Fernández‐Hernando C, Suárez Y. Macrophage deficiency of miR‐21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis. EMBO Molecular Medicine 2017, 9: 1244-1262. PMID: 28674080, PMCID: PMC5582411, DOI: 10.15252/emmm.201607492.Peer-Reviewed Original ResearchConceptsER stress-induced apoptosisPost-translational degradationFoam cell formationMiR-21MiR-21 target genesTarget genesJNK signalingPlaque necrosisAbundant miRNAVascular inflammationAccumulation of lipidsHematopoietic cellsMacrophage apoptosisCell formationAberrant expressionMacrophage deficiencyApoptosisCholesterol effluxProgression of atherosclerosisChronic inflammatory diseasePathophysiological processesInflammatory cellsExpressionInflammatory diseasesCardiovascular diseaseLanosterol Modulates TLR4-Mediated Innate Immune Responses in Macrophages
Araldi E, Fernández-Fuertes M, Canfrán-Duque A, Tang W, Cline GW, Madrigal-Matute J, Pober JS, Lasunción MA, Wu D, Fernández-Hernando C, Suárez Y. Lanosterol Modulates TLR4-Mediated Innate Immune Responses in Macrophages. Cell Reports 2017, 19: 2743-2755. PMID: 28658622, PMCID: PMC5553565, DOI: 10.1016/j.celrep.2017.05.093.Peer-Reviewed Original ResearchConceptsToll-like receptor 4Activator of transcriptionCholesterol biosynthetic pathwayTranscriptional repressionBiosynthetic pathwayLanosterol accumulationGene productsSterol intermediatesSignal transducerGene expressionSelective regulatorSTAT2 activationInnate immune responseType I interferonConditional disruptionCritical functionsMembrane fluidityROS productionMacrophage immunityListeria monocytogenes infectionResistance of miceMouse macrophagesInnate immunityI interferonCYP51A1
2016
ANGPTL4 deficiency in haematopoietic cells promotes monocyte expansion and atherosclerosis progression
Aryal B, Rotllan N, Araldi E, Ramírez CM, He S, Chousterman BG, Fenn AM, Wanschel A, Madrigal-Matute J, Warrier N, Martín-Ventura JL, Swirski FK, Suárez Y, Fernández-Hernando C. ANGPTL4 deficiency in haematopoietic cells promotes monocyte expansion and atherosclerosis progression. Nature Communications 2016, 7: 12313. PMID: 27460411, PMCID: PMC4974469, DOI: 10.1038/ncomms12313.Peer-Reviewed Original ResearchMeSH KeywordsAngiopoietin-Like Protein 4AnimalsApoptosisAtherosclerosisBone Marrow TransplantationCell ProliferationCell SurvivalDisease ProgressionFoam CellsHematopoietic Stem CellsHumansInflammationLeukocytosisMacrophagesMaleMiceMice, Inbred C57BLModels, BiologicalMonocytesMyeloid Progenitor CellsPlaque, AtheroscleroticConceptsFoam cell formationMyeloid progenitor cell expansionANGPTL4 deficiencyCell formationMacrophage gene expressionLipid raft contentMyeloid progenitor populationsProgenitor cell expansionUpregulated genesProgenitor populationsGene expressionHaematopoietic cellsCell surfaceMacrophage apoptosisCell expansionCells resultsProtein 4Lipid accumulationCD36 expressionLike protein 4ExpressionProfound effectMacrophagesGenesLarger atherosclerotic plaques
2015
miR-27b inhibits LDLR and ABCA1 expression but does not influence plasma and hepatic lipid levels in mice
Goedeke L, Rotllan N, Ramírez CM, Aranda JF, Canfrán-Duque A, Araldi E, Fernández-Hernando A, Langhi C, de Cabo R, Baldán Á, Suárez Y, Fernández-Hernando C. miR-27b inhibits LDLR and ABCA1 expression but does not influence plasma and hepatic lipid levels in mice. Atherosclerosis 2015, 243: 499-509. PMID: 26520906, PMCID: PMC4975922, DOI: 10.1016/j.atherosclerosis.2015.09.033.Peer-Reviewed Original ResearchMeSH Keywords3' Untranslated RegionsAdaptor Proteins, Signal TransducingAnimalsATP Binding Cassette Transporter 1BiomarkersChlorocebus aethiopsCholesterolComputational BiologyCOS CellsDatabases, GeneticDiet, High-FatGene Expression RegulationGene Regulatory NetworksHep G2 CellsHumansLiverMacaca mulattaMaleMice, Inbred C57BLMicroRNAsReceptors, LDLTime FactorsTransfectionTriglyceridesConceptsWild-type miceHepatic lipid levelsMiR-27b expressionLipid levelsHepatic lipidsABCA1 expressionMiR-27bWeeks of treatmentExpression of ABCA1Potential therapeutic targetABCA1 protein levelsCellular cholesterol effluxMiR-27b functionsMiR-27b overexpressionMouse hepatic cellsHepatic LDLRHepatic ABCA1Human hepatic Huh7 cellsHepatic cholesterolWestern dietCardiovascular diseaseTherapeutic administrationLDLR expressionTreatment groupsCholesterol efflux
2014
Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis
Rodlan N, Chamorro‐Jorganes A, Araldi E, Wanschel AC, Aryal B, Aranda JF, Goedeke L, Salerno AG, Ramírez CM, Sessa WC, Suárez Y, Fernández‐Hernando C. Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis. The FASEB Journal 2014, 29: 597-610. PMID: 25392271, PMCID: PMC4314230, DOI: 10.1096/fj.14-262097.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtherosclerosisBlood GlucoseBone Marrow CellsBone Marrow TransplantationCell MovementCholesterolCytokinesDisease ProgressionInflammationInsulinLeukocytesLipidsLipoproteins, LDLMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMicroscopy, ConfocalMicroscopy, FluorescencePlaque, AtheroscleroticProto-Oncogene Proteins c-aktReceptors, LDLConceptsProgression of atherosclerosisSerine-threonine protein kinaseBone marrow cellsAkt2-deficient miceInsulin-responsive tissuesWild-type bone marrow cellsProtein kinaseMarrow cellsAkt2 deficiencyAkt2Higher plasma lipidsWild-type miceMice resultsProatherogenic cytokinesObese subjectsPlasma lipidsProinflammatory cytokinesInsulin resistanceInflammatory responseGlucose levelsAtherosclerotic plaquesCholesterol metabolismAtherosclerosisMacrophage migrationMarked reductionLong‐term therapeutic silencing of miR‐33 increases circulating triglyceride levels and hepatic lipid accumulation in mice
Goedeke L, Salerno A, Ramírez CM, Guo L, Allen RM, Yin X, Langley SR, Esau C, Wanschel A, Fisher EA, Suárez Y, Baldán A, Mayr M, Fernández-Hernando C. Long‐term therapeutic silencing of miR‐33 increases circulating triglyceride levels and hepatic lipid accumulation in mice. EMBO Molecular Medicine 2014, 6: 1133-1141. PMID: 25038053, PMCID: PMC4197861, DOI: 10.15252/emmm.201404046.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDiet, High-FatFatty LiverGene SilencingLipid MetabolismLiverMaleMice, Inbred C57BLMicroRNAsOligonucleotides, AntisenseTriglyceridesConceptsHigh-fat dietFatty acid synthaseMiR-33Chronic inhibitionTriglyceride levelsTherapeutic silencingHigh-density lipoprotein levelsAcetyl-CoA carboxylaseLipid accumulationAtherosclerotic vascular diseaseHepatic lipid accumulationRegression of atherosclerosisModerate hepatic steatosisLiver of miceNon-human primatesLipoprotein levelsHepatic steatosisVascular diseaseLong-term effectsStrong inverse correlationPersistent inhibitionVivo increaseCholesterol transportMiceAdverse effectsImproved repair of dermal wounds in mice lacking microRNA‐155
van Solingen C, Araldi E, Chamorro‐Jorganes A, Fernández‐Hernando C, Suárez Y. Improved repair of dermal wounds in mice lacking microRNA‐155. Journal Of Cellular And Molecular Medicine 2014, 18: 1104-1112. PMID: 24636235, PMCID: PMC4112003, DOI: 10.1111/jcmm.12255.Peer-Reviewed Original ResearchConceptsMiR-155Wound tissueWound healingIncreased expressionWound closureImpaired wound repairAnalysis of woundsSkin of miceMiR-155 targetsType 1 collagenWild-type animalsInflammatory mediatorsWT miceWound healing processImmune responseInterleukin-4Healthy skinMicroRNA-155Punch woundsMiceElevated numbersBeneficial effectsWound closingDermal wound healingDermal wounds