Enhanced expression of factor XII (Hageman factor) in isolated livers of estrogen- and prolactin-treated rats

Estrogens and prolactin may raise the plasma titer of factor XII (Hageman factor) by enhancing gene expression at the level of transcription and RNA processing, protein synthesis, or secretion (or a combination of these). Alternatively, these hormones may protect factor XII or its transcripts from degradation. Because the liver is a major site of factor XII synthesis, we studied the expression and metabolism of factor XII in isolated livers of estrogen- and prolactin-treated rats. All rats were ovariectomized to reduce the effect of endogenous estrogen and prolactin on the expression of factor XII. When a phosphorus 32-labeled factor XII complementary DNA probe for Northern blot analysis was used, increased factor XII messenger RNA was found in poly (A) RNA prepared from livers of estrogen- and prolactin-treated rats relative to those of untreated rats. Simultaneously, enhanced release of immunoreactive factor XII was noted when isolated liver perfusion techniques were used. Cycloheximide, an inhibitor of protein synthesis, blocked the hepatic release of immunoreactive factor XII in both hormone-treated and untreated rats, suggesting that factor XII translation was directly affected. The biologic half-life of injected rat iodine 125-labeled factor XII in estradiol- and prolactin-treated rats was not significantly different from that in untreated rats. By inference from these data, the high plasma titer of factor XII observed in estrogen- and prolactin-treated rats is caused by enhanced hepatic expression at both transcriptional and translational levels, as well as by increased secretion of factor XII.