2022
Cell Cycle and Senescence Regulation by Podocyte Histone Deacetylase 1 and 2
Rangel P, Cross E, Liu C, Pedigo C, Tian X, Gutiérrez-Calabrés E, Nagata S, Priyadarshini A, Lerner G, Bunda P, Perincheri S, Gu J, Zhao H, Wang Y, Inoue K, Ishibe S. Cell Cycle and Senescence Regulation by Podocyte Histone Deacetylase 1 and 2. Journal Of The American Society Of Nephrology 2022, 34: 433-450. PMID: 36414418, PMCID: PMC10103311, DOI: 10.1681/asn.2022050598.Peer-Reviewed Original ResearchConceptsCell cycle entryDNA damageSenescence-associated β-galactosidase activityDouble knockout miceRole of HDACsNormal glomerular filtration barrierAssociated phenotypesP21-mediated cell cycle arrestOpen chromatin conformationGlomerular filtration barrierSevere proteinuriaKidney failureProinflammatory cytokinesCell cycle regulationHistone deacetylase 1Cell cycle arrestKi67 expressionSustained DNA damagePodocyte lossIntact expressionMice leadsPodocyte-specific lossMatrix metalloproteinasesPodocyte detachmentProteinuria
2021
Toll-like receptor 7 deficiency suppresses type 1 diabetes development by modulating B-cell differentiation and function
Huang J, Peng J, Pearson JA, Efthimiou G, Hu Y, Tai N, Xing Y, Zhang L, Gu J, Jiang J, Zhao H, Zhou Z, Wong FS, Wen L. Toll-like receptor 7 deficiency suppresses type 1 diabetes development by modulating B-cell differentiation and function. Cellular & Molecular Immunology 2021, 18: 328-338. PMID: 33432061, PMCID: PMC8027372, DOI: 10.1038/s41423-020-00590-8.Peer-Reviewed Original ResearchConceptsType 1 diabetes developmentToll-like receptorsType 1 diabetesDiabetes developmentB cellsTLR7 deficiencyNOD miceB cell differentiationT cellsClassical MHC class I moleculesHuman type 1 diabetesImmunodeficient NOD miceNOD B cellsDiabetogenic T cellsAntigen-presenting functionNonobese diabetic (NOD) miceT cell responsesB cell functionMHC class I moleculesPattern recognition receptorsT cell activationPathogen molecular patternsClass I moleculesDiabetogenic CD4Cytotoxic CD8
2019
Expression of the type 3 InsP3 receptor is a final common event in the development of hepatocellular carcinoma
Guerra MT, Florentino RM, Franca A, Lima Filho AC, Dos Santos ML, Fonseca RC, Lemos FO, Fonseca MC, Kruglov E, Mennone A, Njei B, Gibson J, Guan F, Cheng YC, Ananthanarayanan M, Gu J, Jiang J, Zhao H, Lima CX, Vidigal PT, Oliveira AG, Nathanson MH, Leite MF. Expression of the type 3 InsP3 receptor is a final common event in the development of hepatocellular carcinoma. Gut 2019, 68: 1676. PMID: 31315892, PMCID: PMC7087395, DOI: 10.1136/gutjnl-2018-317811.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsApoptosisCalcium SignalingCarcinogenesisCarcinoma, HepatocellularCell ProliferationCells, CulturedDNA MethylationFemaleGene Expression Regulation, NeoplasticHepatocytesHumansInositol 1,4,5-Trisphosphate ReceptorsLiverLiver NeoplasmsLiver RegenerationMaleMice, KnockoutMiddle AgedSurvival AnalysisConceptsChronic liver diseaseITPR3 expressionLiver cancer cellsLiver diseaseMouse modelFinal common eventCancer cellsSpecimens of patientsIndependent patient cohortsControl liver specimensHuman HCC cellsType 3 InsP3 receptorHuman liver samplesIncreased expression levelCancer deathPatient cohortCommon molecular eventPoor survivalHepatocellular carcinomaLiver specimensNormal liverHCC cellsAbstractTextHCCType 3 isoform