Regulation of factor IXa in vitro in human and mouse plasma and in vivo in the mouse. Role of the endothelium and the plasma proteinase inhibitors.

Regulation of factor IXa in vitro in human and mouse plasma and in vivo in the mouse. Role of the endothelium and the plasma proteinase inhibitors.
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人和小鼠血浆中因子 IXa 的体外调节以及小鼠体内因子 IXa 的调节。

DOI:
10.1172/jci111377
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发表时间:
1984
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
Pizzo,SV
Pizzo,SV
中科院分区:
--
文献类型:
--
作者:
Fuchs,HE;Trapp,HG;Griffith,MJ;Roberts,HR;Pizzo,SV

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在体外、小鼠血浆和小鼠体内研究了人因子IXa的调节作用。在人血浆中,大约60%的125I-Factor IXa在2小时内与抗凝血酶III (ATIII)结合,而不与α 2-巨球蛋白或α 1-蛋白酶抑制剂结合,通过凝胶电泳和IgG-抗蛋白酶抑制剂- sepharose beads进行评估。在肝素存在的情况下,几乎100%的125i -因子IXa在1分钟内与ATIII结合。125i -因子IXa在小鼠血浆中的分布相似。125I-Factor IXa的清除是快速的(2分钟内清除50%)和双相的,并且被大量的atiii -凝血酶和α 1-蛋白酶抑制剂-胰蛋白酶抑制,但不被α 2-大球蛋白-胰蛋白酶抑制;大摩尔过量的二异丙基磷酰- (DIP-) Xa因子、DIP-凝血酶和凝血酶IX因子也能抑制它,但不受凝血酶原或X因子的抑制。因子IX的清除也很快(2.5分钟内清除50%),并且被大摩尔过量的因子IX抑制,但不被大摩尔过量的因子X、凝血酶原、DIP- Xa因子或DIP-凝血酶抑制。电泳和IgG-抗蛋白酶抑制剂- sepharose bead研究证实,注射到小鼠循环2min后,60%的125i -因子IXa与ATIII结合。125I-Factor IXa的器官分布研究表明,大部分放射性在肝脏。这些研究表明,IXa因子与内皮细胞上至少两类结合位点结合。一个位点显然能识别因子IX和IXa,但不能识别因子X、因子Xa、凝血酶原或凝血酶。另一个位点识别凝血酶,因子Xa和因子IXa,但不识别这些凝血因子的酶原形式。结合后,因子IXa与ATIII结合,该复合物被肝细胞从循环中清除。图片
The regulation of human Factor IXa was studied in vitro in human and mouse plasma and in vivo in the mouse. In human plasma, approximately 60% of the 125I-Factor IXa was bound to antithrombin III (ATIII) by 2 h, with no binding to alpha 2-macroglobulin or alpha 1-proteinase inhibitor, as assessed by gel electrophoresis and IgG- antiproteinase inhibitor-Sepharose beads. In the presence of heparin, virtually 100% of the 125I-Factor IXa was bound to ATIII by 1 min. The distribution of 125I-Factor IXa in mouse plasma was similar. The clearance of 125I-Factor IXa was rapid (50% clearance in 2 min) and biphasic and was inhibited by large molar excesses of ATIII-thrombin and alpha 1-proteinase inhibitor-trypsin, but not alpha 2-macro-globulin-trypsin; it was also inhibited by large molar excesses of diisopropylphosphoryl - (DIP-) Factor Xa, DIP-thrombin, and Factor IX, but not by prothrombin or Factor X. The clearance of Factor IX was also rapid (50% clearance in 2.5 min) and was inhibited by a large molar excess of Factor IX, but not by large molar excesses of Factor X, prothrombin, DIP-Factor Xa, or DIP-thrombin. Electrophoresis and IgG- antiproteinase inhibitor-Sepharose bead studies confirmed that by 2 min after injection into the murine circulation, 60% of the 125I-Factor IXa was bound to ATIII. Organ distribution studies with 125I-Factor IXa demonstrated that most of the radioactivity was in the liver. These studies suggest that Factor IXa binds to at least two classes of binding sites on endothelial cells. One site apparently recognizes both Factors IX and IXa, but not Factor X, Factor Xa, prothrombin, or thrombin. The other site recognizes thrombin, Factor Xa, and Factor IXa, but not the zymogen forms of these clotting factors. After this binding, Factor IXa is bound to ATIII and the complex is cleared from the circulation by hepatocytes.Images
用于分离人血浆凝血因子 II、IX 和 X 的硫酸化葡聚糖珠的合成。
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发表时间: 1980
影响因子: 2.9
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抗凝血酶 III 和抗凝血酶 III 复合物的体内代谢。
DOI: --
发表时间: 1982
期刊: The Journal of biological chemistry
影响因子: --
作者:
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发表时间: 1982
期刊: The Journal of biological chemistry
影响因子: --
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DOI: 10.1016/s0021-9258(19)68276-1
发表时间: 1982-01
期刊: The Journal of biological chemistry
影响因子: --
作者:
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通讯作者: N. Esmon;W. Owen;C. Esmon
DOI: --
发表时间: 1978
影响因子: 15.9
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