Coughlin S R, Moskowitz M A, Zetter B R, Antoniades H N, Levine L
Nature. 1980 Dec 11;288(5791):600-2. doi: 10.1038/288600a0.
Prostacyclin (PGI2), an unstable metabolite of arachidonic acid synthesized by vascular endothelial and smooth muscle cells, is a potent vasodilator and endogenous inhibitor of platelet aggregation. Regulation of PGI synthesis by the vessel wall is not well understood. We have investigated the possibility that a product released from platelet granules during degranulation might modify vessel wall PGI2 biosynthesis. We report here that a non-dialysable, platelet-dependent factor in serum dramatically stimulates PGI2 synthesis by cultured bovine aortic endothelium aortic smooth muscle, and adrenal capillary endothelium. Platelet-derived growth factor (PDGF), a releasable peptide contained within platelet alpha granules, stimulates PGI2 synthesis by the above cell types as much as 100-fold. The concentrations of PDGF required to produce these effects are below the level reported in normal human serum. We postulate that in vivo released PDGF may increase vessel wall PGI2 production as part of a negative feedback mechanism controlling platelet aggregation.
前列环素（PGI2）是由血管内皮细胞和平滑肌细胞合成的花生四烯酸的不稳定代谢产物，是一种强效血管扩张剂和血小板聚集的内源性抑制剂。血管壁对PGI合成的调节尚不清楚。我们研究了血小板脱颗粒过程中从血小板颗粒释放的一种产物可能改变血管壁PGI2生物合成的可能性。我们在此报告，血清中一种不可透析的、依赖血小板的因子能显著刺激培养的牛主动脉内皮细胞、主动脉平滑肌细胞和肾上腺毛细血管内皮细胞合成PGI2。血小板衍生生长因子（PDGF）是血小板α颗粒中含有的一种可释放肽，能刺激上述细胞类型合成PGI2达100倍之多。产生这些效应所需的PDGF浓度低于正常人血清中报道的水平。我们推测，体内释放的PDGF可能作为控制血小板聚集的负反馈机制的一部分，增加血管壁PGI2的产生。
