Interferon enhances prostacyclin production by cultured vascular endothelial cells.
Interferon enhances prostacyclin production by cultured vascular endothelial cells.
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干扰素增强培养的血管内皮细胞产生前列环素。
DOI：
10.1172/jci111198
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Panet,A
中科院分区：
文献类型：
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作者：
Eldor,A;Fridman,R;Vlodavsky,I;Hy-Am,E;Fuks,Z;Panet,A
研究了干扰素（IFN）对花生四烯酸代谢以及培养的内皮细胞和血小板的生理功能的影响。研究发现，培养的牛主动脉内皮细胞对人白细胞 (α) IFN 的抗病毒和抗增殖活性敏感，并在暴露于 IFN 后增加其合成前列环素 (PGI2) 的能力。一些观察结果表明，IFN 在磷脂酶 A2 和环氧合酶水平上刺激 PGI2 合成：（a）PGI2 的产生取决于外源花生四烯酸的供应或离子载体 A23187 释放内源细胞花生四烯酸，但当 IFN 处理的细胞暴露于内过氧化物前列腺素 H2 时没有观察到。 (b) 孵育期间（24-72 小时），IFN 对 PGI2 自发释放到培养基中没有影响。 (c) IFN 对 PGI2 产生的刺激作用被糖皮质激素和吲哚美辛抑制。还研究了干扰素对血小板前列腺素代谢的影响。富含血小板的血浆与 IFN 一起孵育对血小板聚集和血栓素 A2 的产生没有影响。鉴于 PGI2 在血管壁中的保护作用以及某些病毒感染在人和实验动物模型中诱导内皮损伤的事实，可以考虑本文提出的研究结果的生物学意义。
The effects of interferon (IFN) on the arachidonate metabolism and physiological functions of cultured endothelial cells and blood platelets have been examined. Cultured bovine aortic endothelial cells were found to be sensitive to the antiviral and antiproliferative activities of human leukocyte (alpha) IFN and to increase their capacity to synthesize prostacyclin (PGI2) upon exposure to IFN. Several observations indicate that IFN stimulates PGI2 synthesis at the level of the enzymes phospholipase A2 and cyclooxygenase: (a) PGI2 production was dependent upon the supply of exogenous arachidonic acid or the liberation of endogenous cellular arachidonate by ionophore A23187, but was not observed when IFN-treated cells were exposed to the endoperoxide prostaglandin H2. (b) IFN had no effect on the spontaneous release of PGI2 into the culture medium during the incubation period (24-72 h). (c) The stimulatory effect of IFN on PGI2 production was inhibited by both glucocorticoids and indomethacin. The effect of IFN on platelet prostaglandin metabolism was also investigated. Incubation of platelet-rich plasma with IFN had no effect on platelet aggregation and thromboxane A2 production. The biological significance of the findings presented in this paper may be considered in view of the protective role of PGI2 in the vessel wall and the fact that infection with certain viruses induces endothelial damage both in man and experimental animal models.