2017
The Transcriptomic Signature Of Disease Development And Progression Of Nonalcoholic Fatty Liver Disease
Cazanave S, Podtelezhnikov A, Jensen K, Seneshaw M, Kumar DP, Min HK, Santhekadur PK, Banini B, Mauro AG, M. Oseini A, Vincent R, Tanis KQ, Webber AL, Wang L, Bedossa P, Mirshahi F, Sanyal AJ. The Transcriptomic Signature Of Disease Development And Progression Of Nonalcoholic Fatty Liver Disease. Scientific Reports 2017, 7: 17193. PMID: 29222421, PMCID: PMC5722878, DOI: 10.1038/s41598-017-17370-6.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDisease ProgressionGene Expression ProfilingLiver CirrhosisMaleMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseSignal TransductionConceptsNonalcoholic fatty liver diseaseFatty liver diseaseAdvanced fibrosisLiver diseaseMacrophage activationPathway activationHepatic stellate cell activationFatty liver developmentStellate cell activationOxidative stress pathwaysCell deathAdvanced diseaseMetabolic pathway activationChow dietFatty liverEarly fibrosisFibrogenic pathwaysCell stressSuch miceAnimal modelsCell activationFibrosisMetabolic perturbationsDiseaseOxidative stressTranscriptional Induction of Periostin by a Sulfatase 2–TGFβ1–SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma
Chen G, Nakamura I, Dhanasekaran R, Iguchi E, Tolosa EJ, Romecin PA, Vera RE, Almada LL, Miamen AG, Chaiteerakij R, Zhou M, Asiedu MK, Moser CD, Han S, Hu C, Banini BA, Oseini AM, Chen Y, Fang Y, Yang D, Shaleh HM, Wang S, Wu D, Song T, Lee JS, Thorgeirsson SS, Chevet E, Shah VH, Fernandez-Zapico ME, Roberts LR. Transcriptional Induction of Periostin by a Sulfatase 2–TGFβ1–SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma. Cancer Research 2017, 77: 632-645. PMID: 27872089, PMCID: PMC5429157, DOI: 10.1158/0008-5472.can-15-2556.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkers, TumorBlotting, WesternCarcinoma, HepatocellularCell Adhesion MoleculesChromatin ImmunoprecipitationEnzyme-Linked Immunosorbent AssayGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansImmunohistochemistryKaplan-Meier EstimateLiver NeoplasmsMiceMice, KnockoutNeovascularization, PathologicOligonucleotide Array Sequence AnalysisReal-Time Polymerase Chain ReactionSignal TransductionSmad ProteinsSulfatasesSulfotransferasesTransforming Growth Factor beta1ConceptsHepatocellular carcinomaSulfatase 2Protein periostinMicrovascular densityHCC cellsExtracellular matrix protein periostinTGFβ1/Smad pathwayMetastatic hepatocellular carcinomaLower microvascular densityPoor patient survivalWild-type miceClinical HCC specimensHuman HCC cellsPatient survivalPOSTN levelsAntiangiogenic approachesKO miceRational drug developmentParacrine fashionNumerous tumorsHCC angiogenesisTumor growthEndothelial proliferationTumor angiogenesisHCC specimens
2016
Molecular mechanisms of lipotoxicity and glucotoxicity in nonalcoholic fatty liver disease
Mota M, Banini BA, Cazanave SC, Sanyal AJ. Molecular mechanisms of lipotoxicity and glucotoxicity in nonalcoholic fatty liver disease. Metabolism 2016, 65: 1049-1061. PMID: 26997538, PMCID: PMC4931958, DOI: 10.1016/j.metabol.2016.02.014.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsCCAAT/enhancer-binding homologous proteinNonalcoholic fatty liver diseasePKR-like ER kinaseFatty liver diseaseP53 upregulated modulatorEndoplasmic reticulum stressGlucose intoleranceHepatocellular injuryPharmacological therapyLiver diseaseMetabolic derangementsInsulin resistanceHepatocyte injuryLipotoxic stateC-Jun NH2-terminal kinase 1Exposure of hepatocytesHigh fructoseProtective roleEnergy homeostasisUpregulated modulatorGlucose dietLipotoxicityMitochondrial impairmentOxidative stressReticulum stress
2014
Brivanib Attenuates Hepatic Fibrosis In Vivo and Stellate Cell Activation In Vitro by Inhibition of FGF, VEGF and PDGF Signaling
Nakamura I, Zakharia K, Banini BA, Mikhail DS, Kim TH, Yang JD, Moser CD, Shaleh HM, Thornburgh SR, Walters I, Roberts LR. Brivanib Attenuates Hepatic Fibrosis In Vivo and Stellate Cell Activation In Vitro by Inhibition of FGF, VEGF and PDGF Signaling. PLOS ONE 2014, 9: e92273. PMID: 24710173, PMCID: PMC3977817, DOI: 10.1371/journal.pone.0092273.Peer-Reviewed Original ResearchMeSH KeywordsAlanineAnimalsCarbon Tetrachloride PoisoningCell LineCell ProliferationCell SurvivalCollagen Type ICollagen Type I, alpha 1 ChainFibroblast Growth FactorsHepatic Stellate CellsHumansImmunohistochemistryLiver CirrhosisLiver NeoplasmsMicePlatelet-Derived Growth FactorProtein Kinase InhibitorsSignal TransductionTriazinesVascular Endothelial Growth Factor AConceptsVascular endothelial growth factor receptorHuman hepatic stellate cellsBile duct ligationLiver fibrosisStellate cell activationPlatelet-derived growth factorCell activationHuman hepatic stellate cell activationChronic thioacetamide administrationHepatic stellate cell activationInhibition of VEGFREndothelial growth factor receptorChronic carbon tetrachlorideNovel therapeutic approachesHepatic stellate cellsStellate cell proliferationSmooth muscle actinDifferent animal modelsLX-2 human hepatic stellate cellsGrowth factor receptorHepatic fibrosisBrivanibDuct ligationLiver cancerTherapeutic approaches