2021
Apobec1 complementation factor overexpression promotes hepatic steatosis, fibrosis and hepatocellular cancer
Blanc V, Riordan JD, Soleymanjahi S, Nadeau J, Nalbantoglu I, Xie Y, Molitor EA, Madison BB, Brunt EM, Mills JC, Rubin DC, Ng I, Ha Y, Roberts LR, Davidson NO. Apobec1 complementation factor overexpression promotes hepatic steatosis, fibrosis and hepatocellular cancer. Journal Of Clinical Investigation 2021, 131 PMID: 33445170, PMCID: PMC7773377, DOI: 10.1172/jci138699.Peer-Reviewed Original ResearchConceptsHuman hepatocellular cancerHigh-fructose dietHepatocellular cancerNonalcoholic fatty liver diseaseFatty liver diseaseExpression of mRNALipogenic gene expressionSpontaneous fibrosisAdvanced fibrosisLiver diseaseLiver functionHepatic steatosisInflammatory pathwaysInflammatory responseFed chowLong-term effectsTissue microarrayHepatic proliferationMRNA expressionFactor overexpressionReduced survivalFibrosisOxidative stressExtracellular matrix organizationSteatosis
2014
Intestinal Epithelial HuR Modulates Distinct Pathways of Proliferation and Apoptosis and Attenuates Small Intestinal and Colonic Tumor Development
Giammanco A, Blanc V, Montenegro G, Klos C, Xie Y, Kennedy S, Luo J, Chang SH, Hla T, Nalbantoglu I, Dharmarajan S, Davidson NO. Intestinal Epithelial HuR Modulates Distinct Pathways of Proliferation and Apoptosis and Attenuates Small Intestinal and Colonic Tumor Development. Cancer Research 2014, 74: 5322-5335. PMID: 25085247, PMCID: PMC4167566, DOI: 10.1158/0008-5472.can-14-0726.Peer-Reviewed Original ResearchConceptsTumor burdenSmall intestineFecal bile acid excretionAcute intestinal injuryColitis-associated cancerBile acid excretionBile acid metabolismColonic epithelial cellsAOM-DSSIntestinal deletionIntestinal injuryProapoptotic gene expressionIntestinal cancerCarcinogenesis protocolIntestinal expressionAcid excretionASBT expressionIntestinal tumorigenesisIntestinal growthVillus heightTransgenic modelGenetic deletionMiceExpression of transcriptsHuR gene
2012
Transient Inability to Manage Proteobacteria Promotes Chronic Gut Inflammation in TLR5-Deficient Mice
Carvalho FA, Koren O, Goodrich JK, Johansson ME, Nalbantoglu I, Aitken JD, Su Y, Chassaing B, Walters WA, González A, Clemente JC, Cullender TC, Barnich N, Darfeuille-Michaud A, Vijay-Kumar M, Knight R, Ley RE, Gewirtz AT. Transient Inability to Manage Proteobacteria Promotes Chronic Gut Inflammation in TLR5-Deficient Mice. Cell Host & Microbe 2012, 12: 139-152. PMID: 22863420, PMCID: PMC4310462, DOI: 10.1016/j.chom.2012.07.004.Peer-Reviewed Original ResearchConceptsChronic colitisGenetic influencing factorsTLR5-deficient miceChronic gut inflammationLow-grade inflammationMucosal immune systemInnate immune deficiencyProinflammatory gene expressionWild-type miceContribution of microbiotaTransient high levelsGut inflammationImmune deficiencyIntestinal microbiotaColitisGut microbiotaImmune systemMice displayUnstable microbiotaGut epitheliumTransient inabilityMicrobiotaInflammationBreakdown of homeostasisIncomplete penetranceCytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges
Carvalho F, Nalbantoglu I, Aitken J, Uchiyama R, Su Y, Doho G, Vijay-Kumar M, Gewirtz A. Cytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges. Mucosal Immunology 2012, 5: 288-298. PMID: 22318495, PMCID: PMC3328601, DOI: 10.1038/mi.2012.8.Peer-Reviewed Original ResearchConceptsInflammasome activation resultsDevelopment of colitisDextran sulfate sodiumInnate immune activatorsDetection of flagellinIntestinal gene expressionPredispose miceSulfate sodiumEpithelial injuryIL-18IL-1βImmune activatorsIntestinal homeostasisSevere diseaseFlagellin administrationSalmonella infectionMonoclonal antibodiesSystemic challengesMiceNLRC4Transcription-independent pathwayIntestinal genesAdministrationActivation resultsBacterial flagellin
2011
Interleukin-1β (IL-1β) promotes susceptibility of Toll-like receptor 5 (TLR5) deficient mice to colitis
Carvalho FA, Nalbantoglu I, Ortega-Fernandez S, Aitken JD, Su Y, Koren O, Walters WA, Knight R, Ley RE, Vijay-Kumar M, Gewirtz AT. Interleukin-1β (IL-1β) promotes susceptibility of Toll-like receptor 5 (TLR5) deficient mice to colitis. Gut 2011, 61: 373. PMID: 21646247, DOI: 10.1136/gut.2011.240556.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalCecumColitis, UlcerativeDisease Models, AnimalDisease SusceptibilityGene Expression ProfilingInterleukin-1betaMaleMetagenomeMiceMice, KnockoutMyeloid Differentiation Factor 88Receptors, Interleukin-10Reverse Transcriptase Polymerase Chain ReactionSignal TransductionToll-Like Receptor 5ConceptsToll-like receptor 4T5KO miceGut microbiotaColitis modelIL-1βAbsence of TLR4Toll-like receptor 5 deficient (T5KO) miceAnti-inflammatory cytokine interleukin-10Endogenous anti-inflammatory pathwayToll-like receptor 5Loss of TLR5Anti-inflammatory pathwayIL-10 receptorCytokine interleukin-10Double knockoutIL-10 signalingIL-1 receptorProinflammatory gene expressionWild-type littermatesColitogenic microbiotaSpontaneous colitisUniform colitisSevere colitisImmune dysregulationIntestinal inflammation