RAT PROTEIN-SV-IV (SEMINAL-VESICLE PROTEIN NO-4) ACCELERATES HUMAN BLOOD-COAGULATION IN-VITRO BY SELECTIVE-INHIBITION OF ANTITHROMBIN-III

Citation
B. Dimicco et al., RAT PROTEIN-SV-IV (SEMINAL-VESICLE PROTEIN NO-4) ACCELERATES HUMAN BLOOD-COAGULATION IN-VITRO BY SELECTIVE-INHIBITION OF ANTITHROMBIN-III, Biochemical pharmacology, 48(2), 1994, pp. 345-352
Citations number
40
Categorie Soggetti
Pharmacology & Pharmacy",Biology
Journal title
ISSN journal
00062952
Volume
48
Issue
2
Year of publication
1994
Pages
345 - 352
Database
ISI
SICI code
0006-2952(1994)48:2<345:RP(PNA>2.0.ZU;2-S
Abstract
The seminal vesicle protein No. 4 (SV-IV) secreted from the rat semina l vesicle epithelium, possesses immunosuppressive and anti-inflammator y properties and it is a potent inhibitor of platelet aggregation both in vivo and in vitro. This research aimed to investigate the possible effect of SV-TV on the process of human blood coagulation. Preliminar y experiments showed that the recalcification time (RT) of platelet-po or plasma (PPP) samples, obtained from both normal subjects and patien ts affected by some hemorrhagic disorders, was found to be markedly re duced in the presence of micromolar amounts of SV-IV. It was demonstra ted that the concentration of free antithrombin III (AT III) occurring in blood sera obtained from PPP samples recalcified in the presence o f SV-IV was significantly decreased in comparison with sera obtained f rom PPP recalcified in the absence of SV-IV. It was also shown that PP P treatment with SV-IV significantly reduced the concentration of free AT III without affecting the levels of other plasma serine protease i nhibitors, such as alpha(2)-macroglobulin, alpha(1)-antitrypsin and C- 1-inhibitor. In addition, the RT of PPP treated with a specific rabbit anti-AT III polyclonal antiserum (anti-AT III treated PPP) was not mo dified by SV-IV. These findings were confirmed by the observation that the addition of SV-IV into an in vitro coagulation system, containing pure fibrinogen, alpha-thrombin and AT-III, resulted in complete supp ression of thrombin inhibition by AT III. No other steps of the blood clotting process (prothrombinase complex, factor XIII, fibrinogen conc entration) were affected by SV-IV.