Princen H M, Moshage H J, Emeis J J, de Haard H J, Nieuwenhuizen W, Yap S H
Thromb Haemost. 1985 Apr 22;53(2):212-5.
Previously, we demonstrated that in vivo regulation of liver fibrinogen synthesis occurs via the fibrinogen mRNA level. However, the molecular regulatory mechanism of fibrinogen synthesis is still not well understood. Fibrinogen or fibrin degradation products might play an important role in regulating fibrinogen synthesis. In our present study, we have injected rats intraperitoneally with purified homologous fragments and measured the liver content of mRNA specific coding for fibrinogen. Increased levels of fibrinogen mRNA and elevated plasma fibrinogen concentrations were observed in rats after administration of fibrinogen degradation products X, Y, DEGTA, Dcate or E. Fragment E or E' has a less stimulatory effect than X, Y or Dcate, whereas cross-linked fibrin degradation product D dimer does not increase fibrinogen synthesis. This article reports for the first time a stimulatory effect of the high molecular weight fibrinogen degradation products on fibrinogen synthesis.
此前，我们证明了肝脏纤维蛋白原合成的体内调节是通过纤维蛋白原mRNA水平实现的。然而，纤维蛋白原合成的分子调节机制仍未完全清楚。纤维蛋白原或纤维蛋白降解产物可能在调节纤维蛋白原合成中起重要作用。在我们目前的研究中，我们给大鼠腹腔注射了纯化的同源片段，并测量了纤维蛋白原特异性编码mRNA的肝脏含量。在给予纤维蛋白原降解产物X、Y、DEGTA、Dcate或E后，大鼠体内纤维蛋白原mRNA水平升高，血浆纤维蛋白原浓度也升高。片段E或E'的刺激作用小于X、Y或Dcate，而交联纤维蛋白降解产物D二聚体不会增加纤维蛋白原的合成。本文首次报道了高分子量纤维蛋白原降解产物对纤维蛋白原合成的刺激作用。
