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Transcellular Mechanisms of Endothelial Permeability and Pulmonary Edema

Transcellular Mechanisms of Endothelial Permeability and Pulmonary Edema
内皮通透性和肺水肿的跨细胞机制
批准号：
8059122
负责人：
Asrar B. Malik
金额：
$42.91万
依托单位：
UNIVERSITY OF ILLINOIS AT CHICAGO
依托单位国家：
美国
项目类别：
财政年份：
2011
资助国家：
美国
项目状态：
已结题
起止时间：
2011-03-01 至 2016-02-29
来源：
https://reporter.nih.gov/project-details/8059122
关键词：
Acute Lung InjuryAddressAdherens JunctionAdhesivesAlbuminsBiochemicalCaveolaeCell Surface ReceptorsCellsDataEndocytosisEndothelial CellsEndotheliumFluid BalanceGeneticHomeostasisImageInflammationInflammation MediatorsKnockout MiceLiquid substanceLungMediatingMediator of activation proteinModificationMusNADPH OxidaseOrganellesOxidation-ReductionPathway interactionsPermeabilityPhosphorylationPhysiologicalPrincipal InvestigatorProcessProductionProteinsPulmonary EdemaRegulationRoleSecondary toSignal PathwaySignal TransductionSignaling ProteinSmall Interfering RNAStructureStructure of parenchyma of lungSuperoxidesTestingThrombinVascular Permeabilitiesbasecadherin 5caveolin 1human NOS3 proteininsightlung vascular injurymouse modelnitrationnovelprogramsresponsetranscytosis

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中文摘要
翻译
肺组织液稳态受内皮细胞对白蛋白和液体的通透性调节，从而破坏 内皮屏障的破坏会导致肺水肿。我们建议解决潜在的重要和 小窝信号蛋白内皮小窝蛋白-1与黏附连接蛋白的新关系 (AJS)，已知调节连接的渗透性的结构。我们假设小窝之间的串扰 而AJ，到目前为止已经被独立研究，可能在调节中具有根本性的重要性 AJ渗透率。的关注点
英文摘要
Lung tissue fluid homeostasis is regulated by endothelial permeability to albumin and liquid such that disrupfion of the endothelial barrier leads to pulmonary edema. We propose to address the potentially important and novel relafionship between endothelial caveolin-1, the signaling protein of caveolae, and adherens juncfions (AJs), structures known to regulate permeability of the junctions. We posit that cross-talk between caveolae and AJs, which up to now have been studied independenfiy, may be of fundamental importance in regulafing AJ permeability. The focus of
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