期刊
BIOMATERIALS
卷 27, 期 24, 页码 4325-4332出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.biomaterials.2006.04.001
关键词
blood coagulation; FXII; Hageman factor; contact activation; autoactivation
资金
- NHLBI NIH HHS [5 R01 HL 69965-03] Funding Source: Medline
Contact activation of blood factor XII (FXII, Hageman factor) in neat-buffer solution is shown not to be specific for anionic hydrophilic procoagulants as proposed by the accepted biochemistry of surface activation. Rather, FXII activation in the presence of plasma proteins leads to an apparent specificity for hydrophilic surfaces that is actually due to a relative diminution of the FXII -> FXIIa reaction at hydrophobic surfaces. FXII activation in neat-buffer solution was effectively instantaneous upon contact with either hydrophilic (fully water-wettable clean glass) or hydrophobic (poorly water-wettable silanized glass) procoagulant particles, with greater FXIIa yield obtained by activation with hydrophobic procoagulants. In sharp contrast, both activation rate and yield was found to be significantly attenuated at hydrophobic surfaces in the presence of plasma proteins. Putative FXIIa produced by surface activation with both hydrophilic and hydrophobic procoagulants was shown to hydrolyze blood factor XI (FXI) to the activated form FXIa (FXIIa (FXIIa)(->) FXIa) that causes FXI-deficient plasma to rapidly coagulate. (c) 2006 Elsevier Ltd. All rights reserved.
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