Akatsu Hiroyasu, Ishiguro Masae, Ogawa Norihiro, Kanesaka Takeshi, Okada Noriko, Yamamoto Takayuki, Campbell William, Okada Hidechika
Choju Medical Institute, Fukushimura Hospital, 19-14 Azayamanaka, Noyori, Toyohashi, Aichi 441-8194, Japan.
Microbiol Immunol. 2007;51(5):507-17. doi: 10.1111/j.1348-0421.2007.tb03939.x.
Thrombin-activatable fibrinolysis inhibitor (TAFI) is an anaphylatoxin-inactivating enzyme generated by proteolytic cleavage of its zymogen, and is the same enzyme as that first designated by our group as procarboxypeptidase R (proCPR). TAFI in plasma is presumed to influence vascular disease in its role as a fibrinolysis inhibitor. The activity of TAFI is strongly influenced by genetic polymorphism, especially at amino acids Thr/Ala-147 and Thr/Ile-325. In this study, we analyzed 202 healthy controls who were not on any medication, had no unusual medical history and whose blood data were normal. In a previous report, we established an enzyme-linked immunosorbent assay (ELISA) specific for non-activated TAFI (proCPR), and investigated levels of unactivated TAFI as an estimate of anti-fibrinolytic capacity. In this study, we determined normal Japanese TAFI levels for each age, sex, and genetic polymorphism of Thr/Ala-147 and Thr/Ile-325, and also showed that the TAFI level in young adult women is lower than in aged women.