Identification of RUNX1 as a Mediator of Aberrant Retinal Angiogenesis
Lam JD, Oh DJ, Wong LL, Amarnani D, Park-Windhol C, Sanchez AV, Cardona-Velez J, McGuone D, Stemmer-Rachamimov AO, Eliott D, Bielenberg DR, van Zyl T, Shen L, Gai X, D'Amore PA, Kim LA, Arboleda-Velasquez JF. Identification of RUNX1 as a Mediator of Aberrant Retinal Angiogenesis. Diabetes 2017, 66: db161035. PMID: 28400392, PMCID: PMC5482092, DOI: 10.2337/db16-1035.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAnimalsCell MovementCell ProliferationCore Binding Factor Alpha 2 SubunitDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Diabetic RetinopathyDisease Models, AnimalEndothelial CellsFemaleGlucoseHumansImmunohistochemistryMaleMiceMiddle AgedOxygenRetinaRetinal NeovascularizationRNA, MessengerConceptsAberrant retinal angiogenesisHuman retinal microvascular endothelial cellsProliferative diabetic retinopathyOxygen-induced retinopathyFibrovascular membranesRetinal angiogenesisEndothelial cellsRetinal microvascular endothelial cellsType 2 diabetesRetina of miceMicrovascular endothelial cellsVascular endothelial cellsNeovascular tuftsDiabetic retinopathyTranscription factor 1Common causeRUNX1 inhibitionImmunohistochemical stainingAdult populationHigh glucoseType 1RetinopathyProtein expressionTube formationFactor 1Absence of Alzheimer Disease Neuropathologic Changes in Eyes of Subjects With Alzheimer Disease
Williams EA, McGuone D, Frosch MP, Hyman BT, Laver N, Stemmer-Rachamimov A. Absence of Alzheimer Disease Neuropathologic Changes in Eyes of Subjects With Alzheimer Disease. Journal Of Neuropathology & Experimental Neurology 2017, 76: 376-383. PMID: 28379416, PMCID: PMC7191616, DOI: 10.1093/jnen/nlx020.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseMacular degenerationΒ-amyloidAlzheimer's disease neuropathologic changeAD-related changesAge-matched controlsEyes of subjectsAD-related featuresSeverity of changesAlzheimer changesNeuropathologic changesPathologic findingsAutopsy casesVisual deficitsCommon causeTDP-43Pathology studiesTau proteinExtracellular depositionΑ-synucleinIntracellular accumulationBrainSimilar changesDegenerationDisease