Abstract
Vaginal bleeding and subchorionic hematomas are associated with increased risk of both early and late pregnancy loss. Previous work suggests that thrombin generation may play a pivotal role in development of these complications. Specifically, in human endometrial stromal cells (HESC), thrombin acts via protease-activated receptors (e.g. PAR-1) to induce matrix metalloproteinases (MMPs) and inflammatory factors. Our hypothesis is that thrombin activates MMPs and disrupts expression of genes involved in matrix homeostasis.
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