Amidolytic, procoagulant, and activation-suppressing proteins produced by contact activation of blood factor XII in buffer solution.

Amidolytic, procoagulant, and activation-suppressing proteins produced by contact activation of blood factor XII in buffer solution.
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DOI:
10.1016/j.biomaterials.2011.09.020
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发表时间:
2011-12
期刊:
影响因子:
14
通讯作者:
Vogler, Erwin A.
Vogler, Erwin A.
中科院分区:
工程技术1区
文献类型:
--
作者:
Golas, Avantika;Yeh, Chyi-Huey Joshua;Siedlecki, Christopher A.;Vogler, Erwin A.

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The relative proportions of enzymes with amidolytic or procoagulant activity produced by contact activation of the blood zymogen factor XII (FXII, Hageman factor) in buffer solution depends on activator surface chemistry/energy. As a consequence, chromogenic assay of amidolytic activity (cleavage of amino acid bonds in s-2302 chromogen) does not correlate with the traditional plasma-coagulation-time assay for procoagulant activity (protease activity inducing clotting of blood plasma). Amidolytic activity did not vary significantly with activator-particle surface energy, herein measured as water adhesion tension ; where is pure buffer interfacial tension and θa is the advancing contact angle. By contrast, procoagulant activity varied as a parabolic-like function of τo, high at both hydrophobic and hydrophilic extremes of activator surface energy and falling through a broad minimum within a 20 <τo < 40 mJ/m2 ( 55o <θa < 75o) range, corroborating and expanding previously-published work. It is inferred from these functional assays that an unknown number of protein fragments are produced by contact activation of FXII (a.k.a. autoactivation) rather than just αFXIIa and βFXIIa as popularly believed. Autoactivation products produced by activator particles within the 20 <τo < 40 mJ/m2 (55o <θa < 75o) surface-energy range suppresses production of procoagulant enzymes by activators selected from the hydrophobic or hydrophilic surface-energy extremes through as-yet unknown biophysical chemistry. Suppression proteins may be responsible for the experimentally-observed autoinhibition of the autoactivation reaction.
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