Preeclampsia is a pregnancy complication which threatens the survival of mothers and fetuses. It originates from abnormal placentation

especially insufficient fusion of the cytotrophoblast cells to form the syncytiotrophoblast. In this study

we found that THBS1

a matricellular protein that mediates cell-to-cell and cell-to-matrix interactions

is downregulated during the fusion of primary cytotrophoblast and BeWo cells

but upregulated in the placenta of pregnancies complicated by preeclampsia. Also

THBS1 was observed to interact with CD36

a membrane signal receptor and activator of the cAMP signaling pathway

to regulate the fusion of cytotrophoblast cells. Overexpression of THBS1 inhibited the cAMP signaling pathway and reduced the BeWo cells fusion ratio

while the effects of THBS1 were abolished by a CD36-blocking antibody. Our results suggest that THBS1 signals through a CD36-mediated cAMP pathway to regulate syncytialization of the cytotrophoblast cells

and that its upregulation impairs placental formation to cause preeclampsia. Thus

THBS1 can serve as a therapeutic target regarding the mitigation of abnormal syncytialization and preeclampsia.