Akai T, Kaji T, Hayakawa Y, Hayashi T, Sakuragawa N
Department of Neurosurgery, Faculty Medicine, Toyama Medical and Pharmaceutical University, Japan.
Thromb Res. 1991 Jun 15;62(6):707-16. doi: 10.1016/0049-3848(91)90374-6.
We previously reported that a treatment of cultures of endothelial cells from bovine aorta with thrombin resulted in a less accumulation of glycosaminoglycans (GAG) in the cell layer. In the present study, we found that thrombin-induced decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) such as heparan sulfate was prevented by antithrombin III (AT III) but not by heparin cofactor II (HC II). However, AT III did not show a significant effect on the 35S-GAG accumulation individually. Pretreatment of the cell layer with neither AT III nor HC II showed any preventive effect. When GAG in the cell layer was labeled with both [35S]sulfate and [3H]glucosamine, neither thrombin nor a combination of thrombin with AT III changed the ratio of the radioactivity of 35S to that of 3H. Although thrombin stimulated the release of 35S-GAG from the cell layer, AT III completely prevented the stimulatory effect. In conclusion, it was suggested that AT III may inhibit the thrombin action on GAG metabolism of endothelial cells to prevent thrombosis in vivo.
我们先前报道，用凝血酶处理牛主动脉内皮细胞培养物会导致细胞层中糖胺聚糖（GAG）的积累减少。在本研究中，我们发现抗凝血酶III（AT III）可防止凝血酶诱导的[35S]硫酸盐标记的GAG（35S-GAG）如硫酸乙酰肝素积累减少，但肝素辅因子II（HC II）则不能。然而，AT III单独对35S-GAG积累没有显著影响。用AT III和HC II预处理细胞层均未显示出任何预防作用。当用[35S]硫酸盐和[3H]葡糖胺标记细胞层中的GAG时，凝血酶或凝血酶与AT III的组合均未改变35S与3H放射性的比值。尽管凝血酶刺激了35S-GAG从细胞层的释放，但AT III完全阻止了这种刺激作用。总之，提示AT III可能抑制凝血酶对内皮细胞GAG代谢的作用，从而在体内预防血栓形成。
