Blank M L, Spector A A, Kaduce T L, Lee T C, Snyder F
Biochim Biophys Acta. 1986 May 21;876(3):373-8. doi: 10.1016/0005-2760(86)90022-6.
The metabolism of platelet activating factor (1-[1,2-3H]alkyl-2-acetyl-sn-glycero-3-phosphocholine) and 1-[1,2-3H]alkyl-2-acetyl-sn-glycerol was studied in cultures of human umbilical vein endothelial cells. Human endothelial cells deacetylated 1-[1,2-3H]alkyl-2-acetyl-sn-glycero-3-phosphocholine to the corresponding lyso compound (1-[1,2-3H]alkyl-2-lyso-sn-glycerol-3-phosphocholine) and a portion was converted to 1-[1,2-3H]alkyl-2-acyl(long-chain)-sn-glycero-3-phosphocholine. Lyso platelet activating factor (lyso-PAF) (1-[1,2-3H]alkyl-2-lyso-sn-glycero-3-phosphocholine) was detected in the media very early during the incubation and the amount remained higher than the level of the lyso product observed in the cells. Cellular levels of 1-[1,2-3H]alkyl-2-lyso-sn-glycero-3-phosphocholine were significantly higher than the acylated product (1-[1,2-3H]alkyl-2-acyl(long-chain)-sn-glycero-3-phosphocholine) at all times during the 60-min incubation period, which suggests that the ratio of acetylhydrolase to acyltransferase activities is greater in endothelial cells than in most other cells. When endothelial cells were incubated with 1-[1,2-3H]alkyl-2-acetyl-sn-glycerol, a known precursor of PAF, 1-[1,2-3H]alkyl-sn-glycerol was the major metabolite formed (greater than 95% of the 3H-labeled metabolites during 20- and 40-min incubations). At least a portion of the acetate was removed from 1-[1,2-3H]alkyl-2-acetyl-sn-glycerol by a hydrolytic factor released from the endothelial cells into the medium during the incubations. Only negligible amounts of the total cellular radioactivity (0.2%) was incorporated into platelet activating factor (1-[1,2-3H]alkyl-2-acetyl-sn-glycero-3-phosphocholine); therefore, it is unlikely that the previously observed hypotensive activity of 1-alkyl-2-acetyl-sn-glycerols can be explained on the basis of the conversion to platelet activating factor (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) by endothelial cells. Results of this investigation indicate that endothelial cells play an important role in PAF catabolism. Undoubtedly, the endothelium is important in the regulation of PAF levels in the vascular system.
在人脐静脉内皮细胞培养物中研究了血小板活化因子（1-[1,2-³H]烷基-2-乙酰基-sn-甘油-3-磷酸胆碱）和1-[1,2-³H]烷基-2-乙酰基-sn-甘油的代谢。人内皮细胞将1-[1,2-³H]烷基-2-乙酰基-sn-甘油-3-磷酸胆碱脱乙酰化为相应的溶血化合物（1-[1,2-³H]烷基-2-溶血-sn-甘油-3-磷酸胆碱），并且一部分被转化为1-[1,2-³H]烷基-2-酰基（长链）-sn-甘油-3-磷酸胆碱。在孵育早期就在培养基中检测到了溶血血小板活化因子（lyso-PAF）（1-[1,2-³H]烷基-2-溶血-sn-甘油-3-磷酸胆碱），其含量一直高于在细胞中观察到的溶血产物水平。在60分钟的孵育期间，1-[1,2-³H]烷基-2-溶血-sn-甘油-3-磷酸胆碱的细胞水平在所有时间都显著高于酰化产物（1-[1,2-³H]烷基-2-酰基（长链）-sn-甘油-3-磷酸胆碱），这表明内皮细胞中乙酰水解酶与酰基转移酶活性的比值比大多数其他细胞中的更大。当内皮细胞与PAF的已知前体1-[1,2-³H]烷基-2-乙酰基-sn-甘油一起孵育时，形成的主要代谢产物是1-[1,2-³H]烷基-sn-甘油（在20分钟和40分钟孵育期间，³H标记的代谢产物中超过95%）。在孵育过程中，内皮细胞释放到培养基中的一种水解因子从1-[1,2-³H]烷基-2-乙酰基-sn-甘油中去除了至少一部分乙酸盐。只有可忽略不计的总细胞放射性（0.2%）掺入到血小板活化因子（1-[1,2-³H]烷基-2-乙酰基-sn-甘油-3-磷酸胆碱）中；因此，先前观察到的1-烷基-2-乙酰基-sn-甘油的降压活性不太可能基于内皮细胞将其转化为血小板活化因子（1-烷基-2-乙酰基-sn-甘油-3-磷酸胆碱）来解释。这项研究的结果表明内皮细胞在PAF分解代谢中起重要作用。毫无疑问，内皮在调节血管系统中PAF水平方面很重要。
