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有证据表明,菲茨杰拉德因子可抵消高岭土或鞣花酸对血浆激肽释放酶酰胺分解特性的抑制作用。

Evidence that Fitzgerald factor counteracts inhibition by kaolin or ellagic acid of the amidolytic properties of a plasma kallikrein.

作者信息

Ratnoff O D, Saito H

出版信息

Blood. 1976 Feb;47(2):243-51.

PMID:1244922
Abstract

Fitzgerald trait, an asymptomatic disorder, is associated with abnormalities of surface-mediated plasma reactions, including coagulation via the intrinsic pathway, augmentation of the clot-promoting properties of factor VII, kaolin-mediated fibrinolysis, kinin generation, and enhancement of vascular permeability by diluted plasma (PF/Dil). These abnormalities can be corrected by Fitzgerald factor, an agent probably identical with high molecular weight kininogen found in normal, but not Fitzgerald-trait plasma. Our preparations of Fitzgerald factor possessed a second property. Amidolysis of alpha-N-benzoyl-L-proline-L-phenylalanine-L-arginine-pnitroanilide by a plasma kallikrein (activated Fletcher factor) was inhibited by kaolin or solutions of ellagic acid. Addition of preparations of Fitzgerald factor to kaolin or to solutions of ellagic acid counteracted their inhibitory properties. The action of these preparations was duplicated by solutions of cytochrome C or IgG, suggesting that these agents may inhibit the negative charges of kaolin or ellagic acid. Fitzgerald factor enhanced amidolysis of both normal and Fitzgerald-trait plasmas exposed to kaolin, effects not duplicated by cytochrome C or IgG. Whether or not the two properties of our preparations of Fitzgerald factor are related to the same agent is not yet certain. The relationship between these observations and the biologic role of Fitzgerald factor remains to be investigated.

摘要

菲茨杰拉德特性是一种无症状疾病,与表面介导的血浆反应异常有关,包括通过内源性途径的凝血、因子VII促凝特性的增强、高岭土介导的纤维蛋白溶解、激肽生成以及稀释血浆(PF/ Dil)引起的血管通透性增强。这些异常可通过菲茨杰拉德因子纠正,该因子可能与正常血浆而非菲茨杰拉德特性血浆中发现的高分子量激肽原相同。我们制备的菲茨杰拉德因子具有第二种特性。血浆激肽释放酶(活化的弗莱彻因子)对α-N-苯甲酰-L-脯氨酸-L-苯丙氨酸-L-精氨酸-对硝基苯胺的酰胺水解作用受到高岭土或鞣花酸溶液的抑制。向高岭土或鞣花酸溶液中添加菲茨杰拉德因子制剂可抵消它们的抑制特性。细胞色素C溶液或IgG溶液可重复这些制剂的作用,表明这些试剂可能抑制高岭土或鞣花酸的负电荷。菲茨杰拉德因子增强了暴露于高岭土的正常血浆和菲茨杰拉德特性血浆的酰胺水解作用,细胞色素C或IgG无法重复此效果。我们制备的菲茨杰拉德因子的这两种特性是否与同一种试剂有关尚不确定。这些观察结果与菲茨杰拉德因子的生物学作用之间的关系仍有待研究。

相似文献

1
Evidence that Fitzgerald factor counteracts inhibition by kaolin or ellagic acid of the amidolytic properties of a plasma kallikrein.有证据表明,菲茨杰拉德因子可抵消高岭土或鞣花酸对血浆激肽释放酶酰胺分解特性的抑制作用。
Blood. 1976 Feb;47(2):243-51.
2
The role of prekallikrein and high-molecular-weight kininogen in the contact activation of Hageman factor (factor XII) by sulfatides and other agents.前激肽释放酶和高分子量激肽原在硫酸脑苷脂及其他试剂对哈格曼因子(因子XII)的接触激活中的作用。
J Lab Clin Med. 1983 Oct;102(4):487-99.
3
Purification of high molecular weight kininogen and the role of this agent in blood coagulation.高分子量激肽原的纯化及其在血液凝固中的作用。
J Clin Invest. 1977 Sep;60(3):584-94. doi: 10.1172/JCI108810.
4
The relative amidolytic activity of Hageman factor (factor XII) and its fragments. The effect of high-molecular-weight kininogen and kaolin.哈格曼因子(因子XII)及其片段的相对酰胺水解活性。高分子量激肽原和高岭土的作用。
J Lab Clin Med. 1980 Aug;96(2):267-77.
5
Cleavage of human high molecular weight kininogen markedly enhances its coagulant activity. Evidence that this molecule exists as a procofactor.人高分子量激肽原的裂解显著增强其凝血活性。该分子作为前辅因子存在的证据。
J Clin Invest. 1984 Apr;73(4):954-62. doi: 10.1172/JCI111319.
6
Fujiwara trait: the first case of kininogen deficiency in Japan.
Adv Exp Med Biol. 1979;120B:93-9.
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The evolution of clot-promoting and amidolytic activities in mixtures of Hageman factor (factor XII) and ellagic acid.在接触因子(凝血因子 XII)与鞣花酸混合物中促凝活性和酰胺水解活性的演变。
J Lab Clin Med. 1982 Aug;100(2):248-60.
8
Abnormalities in the contact activation through factor XII in Fujiwara trait: a deficiency in both high and low molecular weight kininogens with low level of prekallikrein.藤原特质中通过因子 XII 的接触激活异常:高分子量和低分子量激肽原均缺乏,且前激肽释放酶水平较低。
Tohoku J Exp Med. 1981 Jan;133(1):67-80. doi: 10.1620/tjem.133.67.
9
Severe Fletcher factor (plasma prekallikrein) deficiency with partial deficiency of Hageman factor (factor XII): report of a case with observation on in vivo and in vitro leukocyte chemotaxis.重度弗莱彻因子(血浆前激肽释放酶)缺乏伴哈格曼因子(因子Ⅻ)部分缺乏:1例报告及体内和体外白细胞趋化性观察
Am J Hematol. 1982 May;12(3):261-70. doi: 10.1002/ajh.2830120308.
10
Inhibition of the activation of Hageman factor (factor XII) by beta 2-glycoprotein I.β2-糖蛋白I对凝血因子XII(哈格曼因子)激活的抑制作用。
J Lab Clin Med. 1988 May;111(5):519-23.

引用本文的文献

1
Cleavage of human high molecular weight kininogen markedly enhances its coagulant activity. Evidence that this molecule exists as a procofactor.人高分子量激肽原的裂解显著增强其凝血活性。该分子作为前辅因子存在的证据。
J Clin Invest. 1984 Apr;73(4):954-62. doi: 10.1172/JCI111319.
2
Potentiation of the function of Hageman factor fragments by high molecular weight kininogen.高分子量激肽原对哈格曼因子片段功能的增强作用。
J Clin Invest. 1977 Jul;60(1):7-17. doi: 10.1172/JCI108770.
3
Activation and function of human Hageman factor. The role of high molecular weight kininogen and prekallikrein.
人凝血因子Ⅻ的激活与功能。高分子量激肽原和前激肽释放酶的作用。
J Clin Invest. 1977 Jul;60(1):18-31. doi: 10.1172/JCI108754.
4
HLA-linked C2 deficiency in a Dutch patient with systemic lupus erythematosus.一名患有系统性红斑狼疮的荷兰患者的HLA连锁C2缺乏症。
J Clin Pathol. 1979 Jun;32(6):528-33. doi: 10.1136/jcp.32.6.528.