Neuroregulatory and neuropathological actions of the ether-phospholipid platelet-activating factor.
Neuroregulatory and neuropathological actions of the ether-phospholipid platelet-activating factor.
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DOI：
10.1126/science.3381103
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发表时间：
1988-06
期刊：
影响因子：
56.9
通讯作者：
E. Kornecki;Y. Ehrlich
中科院分区：
文献类型：
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作者：
E. Kornecki;Y. Ehrlich
血小板活化因子（PAF）是一种天然存在的磷脂，在多种生物学和病理生理学过程中起着重要的介导作用。在PAF与神经元细胞相互作用的这项研究中，发现PAF增加了克隆NG108 - 15和PC12细胞内游离钙离子的水平。这种增加依赖于细胞外钙，并被拮抗性PAF类似物CV-3988和钙内流阻滞剂戊烯胺和地尔硫卓抑制。这种相互作用的功能性后果，揭示了通过测量PAF引起的，Ca2+依赖的分泌的三磷酸腺苷从PC12细胞。NG108 - 15细胞暴露于低浓度的PAF 3至4天诱导神经元分化;高浓度的PAF具有神经毒性。因此，通过影响Ca2+通量，PAF可能在神经元发育中发挥生理作用，并在神经元因创伤、中风或脊髓损伤而暴露于循环因子时发生的变性中发挥病理生理作用。
Platelet-activating factor (PAF) is a naturally occurring phospholipid that serves as a critical mediator in diverse biological and pathophysiological processes. In this study of the interactions of PAF with neuronal cells, it was found that PAF increased the intracellular levels of free calcium ions in cells of the clones NG108-15 and PC12. The increase was dependent on extracellular calcium and was inhibited by the antagonistic PAF analog CV-3988 and by the calcium-influx blockers prenylamine and diltiazem. A functional consequence of this interaction was revealed by measuring a PAF-elicited, Ca2+-dependent secretion of adenosine triphosphate from PC12 cells. Exposure of NG108-15 cells for 3 to 4 days to low concentrations of PAF induced neuronal differentiation; higher concentrations were neurotoxic. Thus, by influencing Ca2+ fluxes, PAF may play a physiological role in neuronal development and a pathophysiological role in the degeneration that occurs when neurons are exposed to circulatory factors as a result of trauma, stroke, or spinal cord injury.