
pmid: 21262438
Bad pregnancy outcomes have been associated with increased activation of the coagulation cascade and inflammation, in particular the activation of the complement cascade. Recent studies have suggested that inflammatory processes modulate thrombogenic pathways and vice versa. We studied the cross-talk between the coagulation and the complement cascade in the pathogenesis of recurrent miscarriages and preeclampsia in mice. We identified tissue factor (TF) as a crucial mediator of fetal and placental damage in mouse models of recurrent miscarriages and preeclampsia. Increased TF expression increases the release of reactive oxygen species and antiangiogenic molecules from inflammatory cells inducing trophoblast damage and bad pregnancy outcomes. We also demonstrated that pravastatin, by downregulating TF expression, prevents miscarriages and the onset of preeclampsia in mice.
Inflammation, Abortion, Habitual, Anticholesteremic Agents, Abortion, 610, Complement System Proteins, Habitual, Thromboplastin, Mice, Pre-Eclampsia, Pregnancy, Animals, Humans, Female, Blood Coagulation, Complement Activation, Pravastatin
Inflammation, Abortion, Habitual, Anticholesteremic Agents, Abortion, 610, Complement System Proteins, Habitual, Thromboplastin, Mice, Pre-Eclampsia, Pregnancy, Animals, Humans, Female, Blood Coagulation, Complement Activation, Pravastatin
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