ENDOTHELIAL CELL PROSTAGLANDIN I(2) AND PLATELET-ACTIVATING FACTOR PRODUCTION

内皮细胞前列腺素 I(2) 和血小板激活因子的产生

• 批准号: 8361456
• 负责人: JANE MCHOWAT
• 金额: $ 1.64万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-01-01 至 2011-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8361456
• 关键词: Arachidonic Acids; Calcium; Cells; Disease; Edema; Endothelial Cells; Endothelium; Epoprostenol; Funding; Grant; Human; Infiltration; Inflammatory; Lead; Lung; Mass Spectrum Analysis; National Center for Research Resources; Phospholipases A; Platelet Activating Factor; Principal Investigator; Production; Research; Research Infrastructure; Resources; Source; United States National Institutes of Health; airway inflammation; biomedical resource; cost; interstitial

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Damage and activation of lung endothelium can lead to interstitial edema, infiltration of inflammatory cells into the interstitium and airways, and production of inflammatory metabolites, all of which propagate airway inflammation in a variety of diseases. We have previously determined that stimulation of human microvascular endothelial cells from lung (HMVEC-L) results in activation of a calcium-independent phospholipase A(2) (iPLA(2)), and this leads to arachidonic acid release and production of prostaglandin I(2) (PGI(2)) and platelet-activating factor (PAF).

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 肺内皮的损伤和活化可导致间质性水肿、炎性细胞浸润到肺泡和气道中以及炎性代谢物的产生，所有这些都在多种疾病中传播气道炎症。我们先前已经确定，刺激来自肺的人微血管内皮细胞（HMVEC-L）导致钙非依赖性磷脂酶A（2）（iPLA（2））活化，这导致花生四烯酸释放和前列腺素I（2）（PGI（2））和血小板活化因子（PAF）的产生。