Abstract
Poor placentation in early pregnancy leads to placental pathogenesis, such as preeclampsia (PE). Understanding the pathogenesis of the disease has been hampered by inaccessibility to early stage placental tissue where the initial causal changes take place. Recently we reported that human embryonic stem cells (hESC) treated with inhibitors of activin A (A83-01) and FGF2 (PD173074) signaling in presence of BMP4 (termed BAP) differentiate unidirectionally into trophoblast (TB) cells, which provide potential in vitro models of early placental development1.
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