The fibrinoids of the human placenta: origin, composition and functional relevance
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Massive perivillous fibrin deposition: Diagnosis, obstetrical features, and treatment
2024, European Journal of Obstetrics and Gynecology and Reproductive BiologyMaternal metabolism influences neural tube closure
2023, Trends in Endocrinology and MetabolismImaging mass cytometry reveals the prominent role of myeloid cells at the maternal-fetal interface
2022, iScienceCitation Excerpt :This decrease is likely caused by the production of fibrinoid tissue secreted by the trophoblasts, whereby they embed themselves. The matrix-type fibrinoid produced by the trophoblast cells is thought to be needed to anchor the placenta to the uterine wall, to prevent bleedings when the placenta detaches at delivery, and to regulate trophoblast invasion by cell surface integrins (Kaufmann et al., 1996). Integrins are important in regulating all aspects of immune cell functioning, both when maintaining homeostasis and during inflammation and regulation (Harjunpää et al., 2019).
Maternal platelets at the first trimester maternal-placental interface – Small players with great impact on placenta development
2022, PlacentaCitation Excerpt :There, maternal platelets and/or their granule-stored factors can have an impact on EMT and invasiveness of EVTs as well as cell columnar fibrinoid deposition. Activation on the villous surface involves perivillous fibrin deposition, which may indirectly contribute to the shaping of placental villi and the intervillous space [50]. In contrast to these normal processes in early pregnancy, excess platelet activation at the villous surface will lead to serious deregulation of the endocrine activity, sterile inflammation and local apoptosis of the syncytiotrophoblast.
Massive perivillous fibrin deposition of the placenta and pregnancy outcome: A retrospective observational study
2022, PlacentaCitation Excerpt :The fibrinoid material in the placenta is shown to be mainly derived from the maternal circulation (as a by-product of endothelial damage), called fibrin-type fibrinoid. A second type of fibrinoid, matrix-type, is probably also a component and is derived from the extravillous trophoblast [18]. Other, perhaps combined mechanisms not clarified to date, beyond known autoimmune status, thrombophilia or defined coagulopathies, might activate a cascade of immune reactions resulting in MPVFD in the placenta, and makes the fetus a second victim.
Pregnancy induced TMA in severe preeclampsia results from complement-mediated thromboinflammation
2021, Human ImmunologyCitation Excerpt :The constricted spiral arteries result in a turbulent high-pressure blood flow that increases mechanical shear stress to the placental villi. The turbulent blood flow into the intervillous space may promote activation of the coagulation cascade within the intervillous space [52]. Disturbance in coagulation pathway is a central symptom of TMA.