DISTINCT RESPONSE TO INFLAMMATORY CYTOKINES IN ARTERIAL

我们在cultured arterial smooth muscle cells （SMC）中测试了前列腺素的生产和cyclooxygenase-2（COX-2）的表达。十二个莫亚莫亚和八个控制细胞的绳子已经被测试了。Moyamoya和控制SMCs之间的前列腺素的稳定状态水平并不存在差异。当细胞被介素-1 β （IL-1 β）刺激时，前列腺素E-D22-D2 （PGE-D22-D2）释放到中间体明显大于控制SMC，而前列腺素和血栓素B2的剂量没有差异。由moyamoya SMCs生产的IL-1 β-诱导的PGE-I-D22-I-D2产品完全被indomethacin或NS-398的补充所阻断。IL-1 β在控制SMC中有明显刺激的细胞迁移和DNA合成，但对Moyamoya SMC有抑制作用。The inhibitory on the growth and migration of moyamoya SMCs were caused by excessive secretion of PGE D22 y D2 and was reversed by indomethacin treatment。免疫荧光研究和西方印迹分析显示了IL-1 β-刺激的moyamoya SMCs中COX-2蛋白表达的大剂量。这些发现表明，moyamoya SMC对炎症刺激产生了反应，从而产生了PGE-D22-D2通过COX-2的激活增加了血管渗透性和退化的血管音调。这使我们能够向Moyamoya病中的血液成分和促进适度思维的发展。

We examined the production of prostanoids and the expression of cyclooxygenase-2 (COX-2) in cultured arterial smooth muscle cells (SMCs) derived from patients with moyamoya disease. Twelve moyamoya and eight control cell strains were examined. The steady-state levels of prostanoids in the culture medium did not differ between moyamoya and control SMCs. When the cells were stimulated by interleukin-1β (IL-1β), prostaglandin EィイD22ィエD2 (PGEィイD22ィエD2) release into the medium was significantly greater from moyamoya SMCs than from control SMCs, while the amounts of prostacyclin and thromboxane B2 did not differ. IL-1β-induced PGEィイD22ィエD2 production by moyamoya SMCs was completely blocked by the addition of indomethacin or NS-398. IL-1β significantly stimulated cell migration and DNA synthesis in control SMCs, but had an inhibitory effect on moyamoya SMCs. The inhibitory effects on the growth and migration of moyamoya SMCs were caused by excessive secretion of PGEィイD22ィエD2 and was reversed by indomethacin treatment. Immunofluorescence studies and Western blot analysis showed greater amounts of COX-2 protein expression in IL-1β-stimulated moyamoya SMCs. These findings suggest that moyamoya SMCs respond to inflammatory stimuli to produce excess amounts of PGEィイD22ィエD2 through the activation of COX-2, which increases vascular permeability and decreases vascular tone. This facilitates the exposure of vessels to blood constituents and promotes the development of intimal thickening in moyamoya disease.