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Decidual Cell‐expressed Tissue Factor in Human Pregnancy and Its Involvement in Hemostasis and Preeclampsia‐related Angiogenesis
Author(s) -
Lockwood Charles J.,
Krikun Graciela,
Caze Rebeca,
Rahman Mizanur,
Buchwalder Lynn F.,
Schatz Frederick
Publication year - 2008
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1434.013
Subject(s) - angiogenesis , preeclampsia , decidua , thrombin , spiral artery , trophoblast , vascular endothelial growth factor , decidual cells , tissue factor , endocrinology , medicine , hemostasis , biology , microbiology and biotechnology , immunology , andrology , chemistry , placenta , pregnancy , fetus , platelet , coagulation , vegf receptors , genetics
During extravascular trophoblast (EVT) invasion of the decidua, thrombin generated from decidual cell–expressed tissue factor (TF) forms a “hemostatic envelope” that protects against hemorrhage during the initial breaching of capillaries by EVTs and subsequent invasion and remodeling of the spiral arteries and arterioles. Preeclampsia, the world's leading cause of fetal and maternal morbidity and mortality, stems from shallow trophoblast invasion leading to incomplete vascular remodeling that impairs uteroplacental blood flow. A considerable subset of cases of preeclampsia is associated with decidual hemorrhage and maternal thrombophilias, which form excess thrombin from decidual cell–expressed TF. Thrombin affects several cell functions by binding to protease‐activated receptors. In first‐trimester decidual cells, thrombin enhances expression of sFlt‐1, which can block the angiogenic effects of vascular endothelial growth factor (VEGF) and placental growth factor. By contrast, thrombin does not affect decidual cell VEGF expression. Thrombin‐enhanced sFlt‐1 expression by decidual cells, the predominant cell type encountered by invading cytotrophoblasts, could promote preeclampsia by interfering with angiogenesis‐dependent vascular remodeling to reduce uteroplacental blood flow.