Decidual cell expressed tissue factor promotes endometrial hemostasis while mediating abruption associated preterm birth


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.

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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.

Conflicts of Interest

The authors declare no conflicts of interest.


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