Constitutive excessive erythrocytosis causes inflammation and increased vascular permeability in aged mouse brain

摘要: Abstract Excessive erythrocytosis results in severely increased blood viscosity that may compromise the vascular endothelium. Using our transgenic mouse model of excessive we previously showed despite altered brain endothelial cell morphology and an activated vasculature, integrity was largely maintained up to 4–5 months age. We now present data showing persistent long-term damage wall during later stages adulthood (9–12 months) a chronic detrimental inflammatory phenotype vessel permeability likely contributes reduced life span erythropoietin overexpressing mouse. In aged animals cells were detected tissue elevated RNA protein levels markers such as IL-6 TNFα observed both plasma. Additionally, expression p53 other pro-apoptotic markers, well decreased Bcl-xL indicated ongoing death within compartment. Finally, abnormally all organs correlation with tight junction occludin adherens β-catenin brain. Thus sustained activation pathways, dysfunction blood–brain barrier disruption.