2021
Identification of a Metabolic, Transcriptomic, and Molecular Signature of Patatin‐Like Phospholipase Domain Containing 3–Mediated Acceleration of Steatohepatitis
Banini BA, Kumar DP, Cazanave S, Seneshaw M, Mirshahi F, Santhekadur PK, Wang L, Guan HP, Oseini AM, Alonso C, Bedossa P, Koduru SV, Min H, Sanyal AJ. Identification of a Metabolic, Transcriptomic, and Molecular Signature of Patatin‐Like Phospholipase Domain Containing 3–Mediated Acceleration of Steatohepatitis. Hepatology 2021, 73: 1290-1306. PMID: 33131062, PMCID: PMC8046714, DOI: 10.1002/hep.31609.Peer-Reviewed Original Research
2020
Knockout of sulfatase 2 is associated with decreased steatohepatitis and fibrosis in a mouse model of nonalcoholic fatty liver disease
Kim TH, Banini BA, Asumda FZ, Campbell NA, Hu C, Moser CD, Shire AM, Han S, Ma C, Krishnan A, Mounajjed T, White TA, Gores GJ, LeBrasseur NK, Charlton MR, Roberts LR. Knockout of sulfatase 2 is associated with decreased steatohepatitis and fibrosis in a mouse model of nonalcoholic fatty liver disease. AJP Gastrointestinal And Liver Physiology 2020, 319: g333-g344. PMID: 32683952, PMCID: PMC7509257, DOI: 10.1152/ajpgi.00150.2019.Peer-Reviewed Original ResearchConceptsFast food dietStandard chow dietWT miceDiet-induced steatohepatitisNonalcoholic steatohepatitisSulfatase 2Hepatic fibrosisMouse modelStandard chow diet ad libitumChow diet ad libitumNonalcoholic fatty liver diseaseDiet-induced mouse modelConditions of overnutritionProtein expressionFatty liver diseasePotential therapeutic mechanismWild-type miceDiet ad libitumThreefold increaseLiver diseaseChow dietKO miceLiver fibrosisSteatohepatitisMurine modelThe extracellular sulfatase SULF2 promotes liver tumorigenesis by stimulating assembly of a promoter-looping GLI1-STAT3 transcriptional complex
Carr RM, Romecin Duran PA, Tolosa EJ, Ma C, Oseini AM, Moser CD, Banini BA, Huang J, Asumda F, Dhanasekaran R, Graham RP, Toruner MD, Safgren SL, Almada LL, Wang S, Patnaik MM, Roberts LR, Fernandez-Zapico ME. The extracellular sulfatase SULF2 promotes liver tumorigenesis by stimulating assembly of a promoter-looping GLI1-STAT3 transcriptional complex. Journal Of Biological Chemistry 2020, 295: 2698-2712. PMID: 31988246, PMCID: PMC7049957, DOI: 10.1074/jbc.ra119.011146.Peer-Reviewed Original ResearchConceptsGLI family zinc finger 1Transcriptional complexTarget genesSer/ThrSTAT3 target genesSULF2 overexpressionZinc finger 1Suppressor of cytokineTyrosine kinase 4Promoter conformationSpecific gene signaturesSTAT3 functionHuman orthologPromoter bindingTranscriptomic analysisConsensus sitesGli1 knockdownTransgenic mice overexpressingSignal transducerTranscription 3Molecular mechanismsFinger 1Kinase 4Hepatocellular carcinoma growthOverexpression
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 ResearchConceptsNonalcoholic 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
A diet-induced animal model of non-alcoholic fatty liver disease and hepatocellular cancer
Asgharpour A, Cazanave SC, Pacana T, Seneshaw M, Vincent R, Banini BA, Kumar DP, Daita K, Min HK, Mirshahi F, Bedossa P, Sun X, Hoshida Y, Koduru SV, Contaifer D, Warncke UO, Wijesinghe DS, Sanyal AJ. A diet-induced animal model of non-alcoholic fatty liver disease and hepatocellular cancer. Journal Of Hepatology 2016, 65: 579-588. PMID: 27261415, PMCID: PMC5012902, DOI: 10.1016/j.jhep.2016.05.005.Peer-Reviewed Original ResearchConceptsNon-alcoholic steatohepatitisNon-alcoholic fatty liver diseaseDiet-induced animal modelsProgressive non-alcoholic steatohepatitisHuman non-alcoholic steatohepatitisFatty liver diseaseHepatocellular cancerLiver diseaseAnimal modelsDiet-induced mouse modelGene signatureHigh-fat dietSimilar histological phenotypesAd libitum consumptionProgressive fibrosisLDL cholesterolChow dietMice fedInsulin resistanceFat dietClinical endpointsHuman NAFLDObesogenic dietPreclinical modelsMouse model
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