Trophoblast invasion of spiral arteries: a novel in vitro model.
نویسندگان
چکیده
Extravillous trophoblasts invade the uterine wall (interstitial invasion) and the spiral arteries (endovascular invasion), replacing the cells of the vessel wall and creating a high-flow low-resistance vessel. We have developed a novel model to allow the interactions between the invading trophoblast cells and the cells of the spiral artery to be directly examined. Unmodified (non-placental bed) spiral arteries were obtained from uterine biopsies at caesarean section. Fluorescently labelled trophoblasts were seeded on top of artery segments embedded in fibrin gels (to study interstitial invasion) or perfused into the lumen of arteries mounted on a pressure myograph (to study endovascular invasion). Trophoblasts were incubated with the vessels for 3-5 days prior to cryo-sectioning. Both interstitial and endovascular interactions/invasion could clearly be detected and a comparison of the extravillous trophoblast cell line, SGHPL-4 and primary first trimester cytotrophoblasts showed both to be invasive in this model. This novel method will prove useful in an area where in vitro studies have been hampered by the lack of suitable models directly examining cellular interactions during invasion.
منابع مشابه
I-6: Remodelling Uterine Spiral Arteries inPregnancy
Background: During the first trimester of pregnancy the uterine spiral arteries that supply blood to the placenta are remodelled, creating heavily dilated conduits lacking maternal vasomotor control. To effect permanent vasodilatation, the internal elastic lamina and medial elastic fibres must be degraded. Failure of remodelling is a key characteristic of the pathological placenta and is though...
متن کاملUterine spiral artery remodeling involves endothelial apoptosis induced by extravillous trophoblasts through Fas/FasL interactions.
OBJECTIVE Invasion of uterine spiral arteries by extravillous trophoblasts in the first trimester of pregnancy results in loss of endothelial and musculoelastic layers. This remodeling is crucial for an adequate blood supply to the fetus with a failure to remodel implicated in the etiology of the hypertensive disorder preeclampsia. The mechanism by which trophoblasts induce this key process is ...
متن کاملPlatelet-derived soluble factors induce human extravillous trophoblast migration and differentiation: platelets are a possible regulator of trophoblast infiltration into maternal spiral arteries.
In early pregnancy, human extravillous trophoblasts (EVTs) invade and remodel maternal arteries. We have previously demonstrated that CCR1 is expressed on perivascular/endovascular trophoblasts and that CCR1 ligands promote EVT migration. In this study, we examined the physiologic roles of platelet-derived chemoattractants on EVT invasion. By immunohistochemistry, maternal platelets were locali...
متن کاملEstablishment of uteroplacental circulation.
Haemochorial placentation, as it occurs in the human and other primate and rodent species, requires a connection of the placenta with supplying maternal (uteroplacental) arteries. Very little is known of the initial stages but endovascular trophoblast invasion seems to represent an essential element for further elaboration of an adequate uteroplacental circulation. In the human, endovascular tr...
متن کاملSoluble HLA-G regulates motility and invasion of the trophoblast-derived cell line SGHPL-4.
BACKGROUND Soluble human leucocyte antigen-G (sHLA-G) is secreted by extravillous trophoblast (EVT) and has roles in regulating immune cells within the decidua. HLA-G expression on EVT increases as they approach uterine spiral arteries and we have suggested that sHLA-G may be important in the remodelling of these vessels. The autocrine role of sHLA-G in regulating trophoblast function at this c...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Placenta
دوره 23 2-3 شماره
صفحات -
تاریخ انتشار 2002