2024
Pla2g12b drives expansion of triglyceride-rich lipoproteins
Thierer J, Foresti O, Yadav P, Wilson M, Moll T, Shen M, Busch-Nentwich E, Morash M, Mohlke K, Rawls J, Malhotra V, Hussain M, Farber S. Pla2g12b drives expansion of triglyceride-rich lipoproteins. Nature Communications 2024, 15: 2095. PMID: 38453914, PMCID: PMC10920679, DOI: 10.1038/s41467-024-46102-4.Peer-Reviewed Original ResearchConceptsEndoplasmic reticulumAccumulation of intracellular lipidsSubcellular localizationTriglyceride-rich lipoproteinsEvolutionary tradeoffsInteraction partnersNascent lipoproteinsFunctional domainsLipoprotein homeostasisPLA2G12BIntracellular lipidsResistant to atherosclerosisMutant miceVertebratesReticulumTriglyceride incorporationLipid secretionCardiovascular disease riskCalcium-dependentExcessive accumulationDisease riskTriglyceride transportLipoproteinTriglyceridesLipid
2021
Skin Fibrosis and Recovery Is Dependent on Wnt Activation via DPP4
Jussila AR, Zhang B, Caves E, Kirti S, Steele M, Hamburg-Shields E, Lydon J, Ying Y, Lafyatis R, Rajagopalan S, Horsley V, Atit RP. Skin Fibrosis and Recovery Is Dependent on Wnt Activation via DPP4. Journal Of Investigative Dermatology 2021, 142: 1597-1606.e9. PMID: 34808238, PMCID: PMC9120259, DOI: 10.1016/j.jid.2021.10.025.Peer-Reviewed Original ResearchConceptsWnt/β-catenin-responsive geneWnt activationExtracellular matrix homeostasisGenetic evidenceHuman fibrotic diseasesLipid-filled cellsFunctional mediatorsExtracellular matrixDermal adipocytesMatrix homeostasisGenetic modelsNew targetsWntKey targetMechanisms of fibrosisFibrotic diseasesTherapeutic avenuesDermal remodelingExtracellular matrix expansionExcessive accumulationRemodelingFibrosis severitySkin fibrosisFibrotic remodelingDPP4 inhibitors
2020
Paradoxical aortic stiffening and subsequent cardiac dysfunction in Hutchinson–Gilford progeria syndrome
Murtada SI, Kawamura Y, Caulk AW, Ahmadzadeh H, Mikush N, Zimmerman K, Kavanagh D, Weiss D, Latorre M, Zhuang ZW, Shadel GS, Braddock DT, Humphrey JD. Paradoxical aortic stiffening and subsequent cardiac dysfunction in Hutchinson–Gilford progeria syndrome. Journal Of The Royal Society Interface 2020, 17: 20200066. PMID: 32453981, PMCID: PMC7276555, DOI: 10.1098/rsif.2020.0066.Peer-Reviewed Original ResearchConceptsHutchinson-Gilford progeria syndromeSubsequent cardiac dysfunctionSmooth muscle functionPulse wave velocityUltra-rare disordersCardiovascular eventsDevastating sequelaeDiastolic dysfunctionSystolic functionCardiac dysfunctionProgeria syndromeVascular functionAortic functionMuscle functionEarly deathMouse modelTherapeutic windowCardiovascular dataBiomechanical phenotypingDysfunctionSyndromeExcessive accumulationBiomechanical functionArterial developmentPressure-related effects
2016
Excessive Adventitial Remodeling Leads to Early Aortic Maladaptation in Angiotensin-Induced Hypertension
Bersi M, Bellini C, Wu J, Montaniel KR, Harrison DG, Humphrey JD. Excessive Adventitial Remodeling Leads to Early Aortic Maladaptation in Angiotensin-Induced Hypertension. Hypertension 2016, 67: 890-896. PMID: 27001298, PMCID: PMC4833633, DOI: 10.1161/hypertensionaha.115.06262.Peer-Reviewed Original ResearchConceptsAngiotensin II infusion modelAngiotensin-Induced HypertensionMost clinical assessmentsIntimal-medial thickeningWild-type miceNormal mechanical functionBlood pressureArterial stiffeningThoracic aortaInflammatory responseClinical assessmentEnd organsExuberant productionBlood flowCentral arteriesAdventitial collagenHypertensionWall stressExcessive accumulationInfusion modelMechanical functionWeeksCollagen resultsInflammationArtery
2015
Rapid depot-specific activation of adipocyte precursor cells at the onset of obesity
Jeffery E, Church CD, Holtrup B, Colman L, Rodeheffer MS. Rapid depot-specific activation of adipocyte precursor cells at the onset of obesity. Nature Cell Biology 2015, 17: 376-385. PMID: 25730471, PMCID: PMC4380653, DOI: 10.1038/ncb3122.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytes, WhiteAdipogenesisAdipose Tissue, WhiteAndrostadienesAnimalsCell ProliferationDiet, High-FatEatingMaleMiceMice, Inbred C57BLMice, KnockoutObesityPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktRandom AllocationTamoxifenWortmanninConceptsWhite adipose tissueAdipocyte precursorsMolecular mechanismsWAT growthNew adipocytesHigh-fat diet feedingCharacteristics of obesityOnset of obesityDistinct molecular mechanismsActivation of adipogenesisAdipocyte precursor cellsWAT massVisceral depotsDiet feedingMale miceAdipose tissueObesityAkt2 pathwayMature adipocytesPrecursor cellsAdipogenesisAdipocytesExcessive accumulationMiceActivation
2009
RAGE-independent autoreactive B cell activation in response to chromatin and HMGB1/DNA immune complexes
Avalos AM, Kiefer K, Tian J, Christensen S, Shlomchik M, Coyle AJ, Marshak-Rothstein A. RAGE-independent autoreactive B cell activation in response to chromatin and HMGB1/DNA immune complexes. Autoimmunity 2009, 43: 103-110. PMID: 20014975, PMCID: PMC2929824, DOI: 10.3109/08916930903384591.Peer-Reviewed Original ResearchConceptsAM14 B cellsB cell activationHMGB1-DNA complexHMGB1-RAGE interactionNuclear DNACell activationAutoreactive B cell activationB cell responsesB cellsDNA immune complexesImmune complexesSoluble formRole of HMGB1DNAAutoreactive B cell responsesCell responsesCell debrisCellsCellular debrisExcessive accumulationRAGE-deficient miceSystemic autoimmune diseaseActivationRole of RAGETLR9-dependent manner
1998
ATP7B (WND) protein
Terada K, Schilsky M, Miura N, Sugiyama T. ATP7B (WND) protein. The International Journal Of Biochemistry & Cell Biology 1998, 30: 1063-1067. PMID: 9785470, DOI: 10.1016/s1357-2725(98)00073-9.Peer-Reviewed Original ResearchConceptsATP7B proteinP-type ATPaseCopper transporterDisease-specific mutationsIntracellular traffickingKb transcriptSpecific mutationsProteinATP7BGenesGenetic disordersRecombinant adenovirusExcessive accumulationCopper metabolismRecent studiesWilson's diseaseExonsGene deliveryTraffickingKbTranscriptsTransportersMutationsATPase
1988
Magnesium Inhibits Ischemia Induced Calcium Accumulation in Hilar Neurones: Possible Effect of Nmda-Receptor
Benveniste H, Diemer N. Magnesium Inhibits Ischemia Induced Calcium Accumulation in Hilar Neurones: Possible Effect of Nmda-Receptor. Advances In Behavioral Biology 1988, 35: 377-377. DOI: 10.1007/978-1-4684-5562-5_40.Peer-Reviewed Original ResearchHilar neuronsCA 1 pyramidal cellsN-methyl-D-aspartate receptorsCalcium accumulationIschemic brain damageExcessive calcium accumulationIschemic changesIschemic damageBrain damageNMDA receptorsPyramidal cellsSelective vulnerabilityHilar neuronesCalcium influxIrreversible morphological changesCalcium conductanceIschemiaMorphological damageExcessive accumulationNeuronsPivotal roleMorphological changesHoursPossible effectsDamage
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