Shimada K, Kobayashi M, Ozawa T
Nihon Ketsueki Gakkai Zasshi. 1989 Dec;52(8):1337-42.
Anticoagulantly active heparin-like glycosaminoglycans are apparently present on the vascular surface. We have tried to modulate heparin-like substances on endothelial cells using an experimental cell culture system. Perturbation of the endothelial proteoglycan metabolism by beta-D-xyloside resulted in a reduced biosynthesis of cell surface heparan sulfate, and impaired antithrombin III binding to endothelial cells in parallel with an inhibition of endothelial cell heparin-like activity. In a separate series of experiments, treatments of endothelial cells with interleukin 1 beta and tumor necrosis factor alpha, physiological mediators of immunologic and inflammatory responses, were shown to cause an inhibition of the synthesis of endothelial cell surface heparan sulfate. The endothelial heparin-like activity was partially diminished by these cytokines, suggesting that cytokine-mediated suppression of heparin-like substance on endothelial cells is another cytokine-inducible endothelial effect affecting coagulation. The modulation of endothelial heparin-like activity by these pharmacological and physiological agents may have pathophysiological implications in thrombosis.
具有抗凝活性的类肝素糖胺聚糖显然存在于血管表面。我们试图利用实验性细胞培养系统来调节内皮细胞上的类肝素物质。β-D-木糖苷对内皮蛋白聚糖代谢的干扰导致细胞表面硫酸乙酰肝素的生物合成减少，抗凝血酶III与内皮细胞的结合受损，同时内皮细胞类肝素活性受到抑制。在另一系列实验中，用白细胞介素1β和肿瘤坏死因子α（免疫和炎症反应的生理介质）处理内皮细胞，结果显示会抑制内皮细胞表面硫酸乙酰肝素的合成。这些细胞因子使内皮类肝素活性部分降低，这表明细胞因子介导的内皮细胞上类肝素物质的抑制是另一种影响凝血的细胞因子诱导的内皮效应。这些药理和生理试剂对内皮类肝素活性的调节可能在血栓形成中具有病理生理学意义。
