THE ACTIVATION OF HUMAN BLOOD-COAGULATION FACTOR-X ON THE SURFACE OF ENDOTHELIAL-CELLS - A COMPARISON WITH VARIOUS VASCULAR CELLS, PLATELETS AND MONOCYTES

THE ACTIVATION OF HUMAN BLOOD-COAGULATION FACTOR-X ON THE SURFACE OF ENDOTHELIAL-CELLS - A COMPARISON WITH VARIOUS VASCULAR CELLS, PLATELETS AND MONOCYTES
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DOI:
10.1111/j.1365-2141.1994.tb04918.x
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发表时间:
1994-06-01
影响因子:
6.5
通讯作者:
VANMOURIK, JA
VANMOURIK, JA
中科院分区:
医学2区
文献类型:
--
作者:
BRINKMAN, HJM;MERTENS, K;VANMOURIK, JA

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将内皮细胞上的 X 因子激活率与其他血管细胞、血小板、单核细胞和带负电的磷脂囊泡的激活率进行比较。在没有细胞扰动剂的情况下,在平滑肌细胞和成纤维细胞上观察到因子 VIIa 介导的因子 X 激活,而内皮细胞需要激活才能允许因子 X 的外源激活。另一方面,未受扰动的内皮细胞确实促进因子 VIII/IXa 依赖性的因子 X 的内在激活。这些细胞上的因子 X 激活率约为离子载体 A23187 刺激的因子 X 激活率的六分之一。血小板。此外,平滑肌细胞和成纤维细胞能够通过内在途径激活 X 因子,尽管程度低于内皮细胞。单核细胞在这方面是无效的。凝血酶原片段 1(含有已知介导维生素 K 依赖性凝血因子与磷脂表面结合的 γ-羧基谷氨酸结构域的凝血酶原片段)抑制内皮细胞上的因子 VIII/IXa 依赖性因子 X 激活(IC50 3.2 μM),其程度低于对磷脂囊泡(IC50 0.2 μM)的抑制程度。因此,除了带负电的磷脂外,其他膜成分似乎也参与内皮细胞介导的因子 X 的内在激活。用佛波醇肉豆蔻酸酯乙酸酯 (PMA) 或脂多糖 (LPS) 扰动内皮细胞对因子 X 的内在激活没有影响。这一观察结果表明,参与因子 VIII/IXa 依赖性激活的内皮细胞的膜成分是组成型表达的。
Rates of factor X activation on endothelial cells were compared with activation rates on other vascular cells, platelets, monocytes and negatively charged phospholipid vesicles. Factor VIIa-mediated factor X activation was observed on smooth muscle cells and fibroblasts in the absence of cell-perturbing agents, whereas endothelial cells required activation in order to allow extrinsic activation of factor X. On the other hand, unperturbed endothelial cells did promote intrinsic, factor VIII/IXa-dependent activation of factor X. The rate of factor X activation on these cells was about one-sixth of that on ionophore A23187-stimulated platelets. Also, smooth muscle cells and fibroblasts were able to activate factor X through the intrinsic pathway, although to a lesser extent than endothelial cells. Monocytes were ineffective in this respect. Prothrombin fragment 1, the prothrombin fragment containing the gamma-carboxyglutamic acid domain known to mediate binding of vitamin K-dependent coagulation factors to phospholipid surfaces, inhibited factor VIII/IXa-dependent factor X activation on endothelial cells (IC50 3.2 mu M) to a lesser extent than on phospholipid vesicles (IC50 0.2 mu M). Therefore, besides negatively charged phospholipids, other membrane constituents seem to be involved in endothelial cell mediated, intrinsic activation of factor X. Perturbation of endothelial cells with phorbol myristate acetate (PMA) or lipopolysaccharide (LPS) was without effect on intrinsic activation of factor X. This observation indicates that membrane constituents of endothelial cells involved in factor VIII/IXa-dependent activation of factor X are constitutively expressed.