ACTIVATION OF GROUP VI PHOSPHOLIPASE A2 ISOFORMS IN CARDIAC ENDOTHELIAL CELLS

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。 内皮包括循环和组织之间的细胞屏障。我们之前已经证明，类胰蛋白酶或凝血酶激活人冠状动脉内皮细胞（HCAEC）表面的蛋白酶激活受体-1（PAR-1）和PAR-2可增加VIA族磷脂酶A2（iPLA 2 <$）的活性，并导致多种磷脂衍生的炎性代谢产物的产生。

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. The endothelium comprises a cellular barrier between the circulation and tissues. We have previously shown that activation of protease-activated receptor-1 (PAR-1) and PAR-2 on the surface of human coronary artery endothelial cells (HCAEC) by tryptase or thrombin increases Group VIA phospholipase A2 (iPLA2¿) activity and results in production of multiple phospholipid-derived inflammatory metabolites.