Shimada K, Kobayashi M, Kimura S, Nishinaga M, Takeuchi K, Ozawa T
Department of Cardiology, Jichi Medical School, Minamikawachi, Tochigi, Japan.
Jpn Circ J. 1991 Oct;55(10):1016-21. doi: 10.1253/jcj.55.1016.
Atherosclerosis is associated with an accumulation of proteoglycans. Proteoglycans and/or glycosaminoglycans, in particular heparan sulfate, produced by endothelial cells are thought to play important roles in diverse vascular functions. Of particular note is that they possess anticoagulant functions, i.e., heparin-like antithrombin cofactor activity. Incubation of antithrombin III with endothelial cell cultures resulted in a specific, saturable binding of this protease inhibitor presumably to the endothelial cell surface. In addition, thrombin inactivation by antithrombin III was accelerated on the endothelial surface, providing strong evidence that heparan sulfate on the surface of endothelial cells exerts a heparin-like activity. beta-D-xyloside or cytokine treatments altered the synthesis of heparan sulfate on the endothelial cell surface, resulting in decreased anti-thrombin III binding and diminished heparin-like anticoagulant activity of endothelial cells. The modulation of endothelial heparin-like compounds by these pharmacologic or physiologic agents may have pathophysiologic implications in thrombosis as well as atherogenesis.
动脉粥样硬化与蛋白聚糖的积累有关。内皮细胞产生的蛋白聚糖和/或糖胺聚糖，特别是硫酸乙酰肝素，被认为在多种血管功能中发挥重要作用。特别值得注意的是，它们具有抗凝功能，即肝素样抗凝血酶辅因子活性。抗凝血酶III与内皮细胞培养物孵育导致这种蛋白酶抑制剂可能特异性、饱和性地结合到内皮细胞表面。此外，抗凝血酶III在内皮表面加速凝血酶失活，有力地证明了内皮细胞表面的硫酸乙酰肝素具有肝素样活性。β-D-木糖苷或细胞因子处理改变了内皮细胞表面硫酸乙酰肝素的合成，导致抗凝血酶III结合减少和内皮细胞肝素样抗凝活性降低。这些药理或生理剂对内皮肝素样化合物的调节可能在血栓形成以及动脉粥样硬化发生中具有病理生理学意义。
