Author(s)

Saeed Faramarzi, Umit A. Kayisli, Ozlem Kayisli, Murat Basar, John Shapiro, Nihan Semerci, Joseph Huang, Longzhu Piao, Frederick Schatz, Charles J. Lockwood

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Department of Obstetrics, Gynecology, Ohio State University School of Medicine, Biomedical Research Tower, Columbus, USA.

During human pregnancy, progesterone induced decidual cells protect against hemorrhage: 1) as endovascular trophoblast breech and remodel uterine blood vessels; and 2) in the third stage of labor following preterm and term delivery. De- cidual cells promote hemostasis through enhanced expression of tissue factor (TF), the primary initiator of hemostasis via thrombin generation, and plasminogen activator inhibitor-1, which inactivates tissue type plasminogen activator, the primary fibrinolytic agent. Abruptions (decidual hemorrhage) produce excess thrombin which acts as autocrine/paracrine inducer of decidual cell expressed matrix metalloproteinases and of neutrophil chemoattractant and activator, interleukin-8. The latter mediates aseptic abruption-related neutrophil infiltration. During abruptions, decidual cell and neutrophil-derived proteases effectively degrade the decidual and fetal membrane extracellular matrix to promote preterm premature rupture of the membranes and preterm delivery (PTD). Decidual cell-derived thrombin weakens the amniotic membrane and lowers decidual cell-expressed progesterone receptor levels by increasing phospho-ERK1/2 signaling. The resulting functional progesterone withdrawal accompanies PTD.

Preterm Birth; Abruption; Hemostasis; Tissue Factor; Thrombin

Faramarzi, S. , A. Kayisli, U. , Kayisli, O. , Basar, M. , Shapiro, J. , Semerci, N. , Huang, J. , Piao, L. , Schatz, F. and J. Lockwood, C. (2013) Decidual cell expressed tissue factor promotes endometrial hemostasis while mediating abruption associated preterm birth. Advances in Reproductive Sciences, 1, 44-50. doi: 10.4236/arsci.2013.13007.