Characterization of the interaction between factor Xa and bovine aortic endothelial cells.
Characterization of the interaction between factor Xa and bovine aortic endothelial cells.
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Xa 因子与牛主动脉内皮细胞之间相互作用的表征。
DOI：
10.1016/0167-4889(85)90133-8
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Shuman,MA
中科院分区：
文献类型：
--
作者：
Rodgers,GM;Shuman,MA
用Xaactivate凝血酶原培养的牛主动脉内皮细胞。由内皮细胞合成的因子V或血浆因子V和钙是反应所必需的。在目前的研究中，已经证明125i -因子特异性地与内皮细胞结合。此外，凝血酶原被xa因子和主动脉内皮细胞激活的研究也得到了进一步的证实。125i -因子xto内皮细胞的结合是饱和和可逆的。125i - factor结合的平衡解离常数（Kd）为3.6·10−9M，每个细胞结合39000个分子。经氟磷酸二异丙基灭活的125i - Xa因子不能特异性地与内皮细胞结合，这表明结合需要Xa因子的活性位点。因子Xa，但没有激活蛋白C，与125i因子Xa竞争结合。细胞裂解物的十二烷基硫酸钠-聚丙烯酰胺凝胶的自射线图表明，与细胞结合的放射性标记物质具有与因子xa α和Xaβ相同的电泳迁移率。虽然因子X部分抑制了125i -因子Xa的结合，但因子xaad不抑制125i -因子X的结合，这表明酶原和酶结合到不同的受体上。在这些研究中测量的125i -因子结合与主动脉内皮细胞凝血酶原活化的关系尚不清楚，因为抗因子V IgG阻断凝血酶原活化，但不阻断因子结合。此外，125I-Factor与非血管细胞结合；这些细胞在Xa因子存在时不能激活凝血酶原。此外，各反应的钙需要量和125i -因子结合和凝血酶原活化的饱和曲线也不同。虽然这些数据不排除因子xabin结合和凝血酶原活化之间的关系，但这些研究中测量的125i -因子xabin与主动脉内皮的结合可能与单独的细胞功能有关。为了进一步表征xa因子和内皮细胞对凝血酶原的激活作用，我们比较了完整的牛主动脉和来源于该组织的内皮细胞的凝血酶生成率，发现两者是相等的。这些数据表明血管内皮可以作为止血的生理表面。
Cultured bovine aortic endothelial cells incubated with Factor Xaactivate prothrombin. Factor V, synthesized by the endothelial cells, or plasma Factor V and calcium are required for the reaction. In the present study, it has been demonstrated that125I-Factor Xabinds specifically to endothelial cells. In addition, the activation of prothrombin by Factor Xaand aortic endothelial cells has been further characterized. The binding of125I-Factor Xato endothelial cells was saturable and reversible. The equilibrium dissociation constant (Kd) for125I-Factor Xabinding was 3.6·10−9M, with 39000 molecules bound per cell.125I-Factor Xa, inactivated by diisopropylfluorophosphate did not bind specifically to endothelial cells, indicating that the active site of Factor Xawas required for binding. Factor Xa, but not activated protein C, competed with125I-Factor Xafor binding. Autoradiograms of sodium dodecyl sulfate-polyacrylamide gels of cell lysates indicated that the radiolabeled material that bound to the cells had electrophoretic mobility identical to Factors Xaαand Xaβ. Although Factor X partially inhibited the binding of125I-Factor Xa, Factor Xadid not inhibit the binding of125I-Factor X, indicating that the zymogen and enzyme bound to different receptors. The relationship of the125I-Factor Xabinding which was measured in these studies to aortic endothelial cell prothrombin activation is unclear since an anti-Factor V IgG blocked prothrombin activation but not Factor Xabinding. Additionally,125I-Factor Xabinds to nonvascular cells; these cells do not activate prothrombin in the presence of Factor Xa. Moreover, the calcium requirements for each reaction and the saturation curves of125I-Factor Xabinding and prothrombin activation differ. Although these data do not exclude a relationship between Factor Xabinding and prothrombin activation, the binding of125I-Factor Xato aortic endothelium measured in these studies may be related to a separate cellular function. To further characterize prothrombin activation by Factor Xaand endothelial cells, the rates of thrombin generation by intact bovine aorta or endothelial cells derived from this tissue were compared and were found to be equivalent. These data indicate that vascular endothelium may serve as a physiologic surface for hemostasis.
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协调因子 Va 和因子 Xa 与未刺激的血小板的结合。
DOI：
--
发表时间：
1981
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Tracy,PB;Nesheim,ME;Mann,KG
通讯作者：
Mann,KG
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作者：
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影响因子：
7.5
作者：
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通讯作者：
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影响因子：
15.9
作者：
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影响因子：
15.9
作者：
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G. Broze