2015
Human adipose tissue expansion in pregnancy is impaired in gestational diabetes mellitus
Rojas-Rodriguez R, Lifshitz L, Bellve K, Min S, Pires J, Leung K, Boeras C, Sert A, Draper J, Corvera S, Moore Simas T. Human adipose tissue expansion in pregnancy is impaired in gestational diabetes mellitus. Diabetologia 2015, 58: 2106-2114. PMID: 26067361, PMCID: PMC4526585, DOI: 10.1007/s00125-015-3662-0.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAdipogenesisAdipose TissueAdiposityAdultBlood GlucoseCapillariesCross-Sectional StudiesDiabetes, GestationalFemaleGene Expression ProfilingGene Expression RegulationGlucose Tolerance TestHumansInsulin-Like Growth Factor Binding Protein 5Insulin-Like Growth Factor IInsulin-Like Growth Factor IINeovascularization, PhysiologicOligonucleotide Array Sequence AnalysisPregnancyReal-Time Polymerase Chain ReactionConceptsGestational diabetes mellitusNormal glucose toleranceDiabetes mellitusCapillary densityAdipocyte sizeType 2 diabetes mellitusMethodsThis cross-sectional studyCapillary growthEctopic lipid depositionIGF binding proteinNon-pregnant womenCross-sectional studyAdipose tissue expansionCaesarean deliveryGlucose tolerancePregnant womenInsulin resistanceAdipocyte hypertrophyAT expansionQuantitative real-time PCRReal-time PCRIGF-1Real-time PCR studiesAims/Lipid deposition
2013
A Role for Uric Acid and the Nalp3 Inflammasome in Antiphospholipid Antibody-Induced IL-1β Production by Human First Trimester Trophoblast
Mulla MJ, Salmon JE, Chamley LW, Brosens JJ, Boeras CM, Kavathas PB, Abrahams VM. A Role for Uric Acid and the Nalp3 Inflammasome in Antiphospholipid Antibody-Induced IL-1β Production by Human First Trimester Trophoblast. PLOS ONE 2013, 8: e65237. PMID: 23762324, PMCID: PMC3675211, DOI: 10.1371/journal.pone.0065237.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, AntiphospholipidAntiphospholipid SyndromeBeta 2-Glycoprotein ICARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Cell LineCytoskeletal ProteinsFemaleGene Expression RegulationHumansInflammasomesInterleukin-1betaMiceNLR Family, Pyrin Domain-Containing 3 ProteinPregnancyPregnancy Trimester, FirstProtein PrecursorsSignal TransductionToll-Like Receptor 4TrophoblastsUric AcidConceptsIL-1β productionIntrauterine growth restrictionIL-1β secretionAntiphospholipid syndromeIL-1β processingAntiphospholipid antibodiesIL-1βHuman first trimester trophoblast cell lineFirst trimester trophoblast cell lineUric acidNalp3/ASC inflammasomeHuman first trimester trophoblast cellsToll-like receptor 4Human first-trimester trophoblastsFirst trimester trophoblast cellsAnti-β2GPI AbsAdverse pregnancy outcomesAnti-β2GPI antibodiesRecurrent pregnancy lossTLR4-dependent mannerApoptosis-associated speck-like proteinMaternal-fetal interfaceFirst trimester trophoblastsSpeck-like proteinTrophoblast cell line
2012
Nod1, but not the ASC inflammasome, contributes to induction of IL-1β secretion in human trophoblasts after sensing of Chlamydia trachomatis
Kavathas PB, Boeras CM, Mulla MJ, Abrahams VM. Nod1, but not the ASC inflammasome, contributes to induction of IL-1β secretion in human trophoblasts after sensing of Chlamydia trachomatis. Mucosal Immunology 2012, 6: 235-243. PMID: 22763410, PMCID: PMC3465624, DOI: 10.1038/mi.2012.63.Peer-Reviewed Original ResearchMeSH KeywordsCARD Signaling Adaptor ProteinsCarrier ProteinsCell LineChlamydia trachomatisCytoskeletal ProteinsGene ExpressionHumansInflammasomesInterleukin-1betaMyeloid Differentiation Factor 88NLR Family, Pyrin Domain-Containing 3 ProteinNod1 Signaling Adaptor ProteinToll-Like Receptor 2Toll-Like Receptor 4TrophoblastsConceptsIL-1β secretionToll-like receptorsCT infectionIL-1βASC inflammasomeChlamydia trachomatisKey Toll-like receptorsNalp3/ASC inflammasomePro-inflammatory cytokinesIL-1β mRNAIL-1β productionInnate immune pathwaysNOD-like receptorsHuman trophoblast cellsIntracellular bacterial pathogenChlamydia infectionImmune pathwaysObligate intracellular bacterial pathogenTrophoblast cellsHuman trophoblastsCaspase-1InfectionSecretionInflammasomeNOD1
2011
Uric Acid Induces Trophoblast IL‐1β Production Via the Inflammasome: Implications for the Pathogenesis of Preeclampsia
Mulla MJ, Myrtolli K, Potter J, Boeras C, Kavathas PB, Sfakianaki AK, Tadesse S, Norwitz ER, Guller S, Abrahams VM. Uric Acid Induces Trophoblast IL‐1β Production Via the Inflammasome: Implications for the Pathogenesis of Preeclampsia. American Journal Of Reproductive Immunology 2011, 65: 542-548. PMID: 21352397, PMCID: PMC3114103, DOI: 10.1111/j.1600-0897.2010.00960.x.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Cell LineCytoskeletal ProteinsDisease ProgressionEnzyme ActivationFemaleGene Expression Regulation, DevelopmentalHumansHyperuricemiaInflammasomesInterleukin-1betaMaternal-Fetal RelationsNLR Family, Pyrin Domain-Containing 3 ProteinNLR ProteinsPre-EclampsiaPregnancyTrophoblastsUric AcidConceptsIL-1β secretionIL-1β productionMonosodium urateTrophoblast cellsUric acidFirst trimester trophoblast cellsAdverse pregnancy outcomesPathogenesis of preeclampsiaMaternal-fetal interfaceInduction of inflammationActive IL-1βNOD-like receptorsThird trimester trophoblastActive caspase-1Uric acid increasesCaspase-1 activationIL-1β processingPregnancy outcomesInflammatory dysregulationPlacental dysfunctionClinical manifestationsIL-1βInflammasome activationNALP3 inflammasomePreeclampsia