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Fig. 3. Coincident with exit from the placental compartment, cytotrophoblasts
switch from a venous to an arterial phenotype, as shown by their modulation of
EPH and ephrin family members. (A-F) In situ hybridization; adjacent sections
were stained with cytokeratin 7 (CK7), which identified trophoblasts. Venular
and arterial endothelial cells (ECs) that lined uterine vessels expressed
EPHB4 (A) and ephrin B2 (B). (C) Cytotrophoblast progenitors (CTB prog.) and
syncytiotrophoblasts (STB) within the placenta expressed EPHB4. Commitment to
the differentiation pathway that gives rise to invasive cytotrophoblasts
(iCTBs) is associated with an abrupt downregulation of EPHB4 and a concomitant
upregulation of ephrin B1 (D) and EPHB2 (E) mRNAs. Subsequently, within the
uterine stroma, ephrin B2 expression is induced (F). The endovascular
subpopulation of invasive cytotrophoblasts that line maternal arteries also
expressed high levels of these molecules (D-F). (G) Schematic diagram of the
human maternal-fetal interface highlighting important aspects of
cytotrophoblast interactions with uterine vessels. The pattern of
cytotrophoblast EPH and ephrin expression is shown in the colors indicated.
(H) Cytotrophoblasts modulated EPH and ephrin expression during
differentiation along the invasive pathway in vitro. Immediately after
isolation from placental chorionic villi, the progenitors expressed EPHB4, but
upregulated ephrin B1, B2 and EPHB2 after 12 hours in culture. IVS,
intervillous space; T, trimester. Scale bars: 50 µm in A,B,F; 100 µm in
C-E.
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