Fisher G J, Talwar H S, Ryder N S, Voorhees J J
Department of Dermatology, University of Michigan Medical Center, Ann Arbor 48109.
Biochem Biophys Res Commun. 1989 Sep 29;163(3):1344-50. doi: 10.1016/0006-291x(89)91126-1.
Treatment of cultured adult human keratinocytes with platelet activating factor (PAF) resulted in a rapid, dose dependent accumulation of inositol phosphates. Inositol trisphosphate (IP3), inositol bisphosphate (IP2) and inositol phosphate (IP) were elevated within 15 seconds of exposure to PAF (1 microM). Lyso-PAF, phosphatidylcholine (PC) and lyso-PC had no effect on levels of inositol phosphates, indicating that the effect of PAF was specific. PAF also raised cellular 1,2-diacylglycerol content (2-fold) within two minutes of addition and stimulated mobilization of arachidonic acid (AA) and release of prostaglandin E2. In contrast, PAF did not stimulate phosphoinositide turnover or AA release in cultured dermal fibroblasts. These results suggest that the inflammatory effects of PAF in human skin result, at least in part, from its ability to directly activate keratinocytes and stimulate release of pro-inflammatory eicosanoids.
用血小板活化因子（PAF）处理培养的成人人类角质形成细胞，会导致肌醇磷酸迅速、剂量依赖性地积累。在暴露于PAF（1微摩尔）的15秒内，三磷酸肌醇（IP3）、二磷酸肌醇（IP2）和肌醇磷酸（IP）升高。溶血PAF、磷脂酰胆碱（PC）和溶血PC对肌醇磷酸水平没有影响，表明PAF的作用具有特异性。添加PAF两分钟内，其还使细胞内1,2 - 二酰基甘油含量增加了两倍，并刺激了花生四烯酸（AA）的动员和前列腺素E2的释放。相比之下，PAF不会刺激培养的真皮成纤维细胞中的磷酸肌醇周转或AA释放。这些结果表明，PAF在人类皮肤中的炎症作用至少部分源于其直接激活角质形成细胞并刺激促炎类花生酸释放的能力。
