RT Journal Article
SR Electronic
T1 The depletion of MARVELD1 leads to placenta accreta via integrin β4-dependent trophoblast cell invasion
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 106807
DO 10.1101/106807
A1 Yue Chen
A1 Hui Zhang
A1 Fang Han
A1 Lei Yue
A1 Chunxiao Qiao
A1 Yao Zhang
A1 Peng Dou
A1 Weizhe Liu
A1 Yu Li
YR 2017
UL http://biorxiv.org/content/early/2017/02/07/106807.abstract
AB The mammalian placenta is a remarkable organ. It serves as the interface between the mother and the fetus. Proper invasion of trophoblast cells into the maternal decidua is required for a successful pregnancy. Previous studies have found that the adhesion molecule integrin β4 plays important roles during trophoblast cell invasion. Here, we found that the overall birth rate of the MARVELD1 knockout mouse is much lower than that of the wild-type mouse (P<0.001). In E18.5 MARVELD1 knockout mice, we observed an over-invasion of trophoblast cells, and indeed, the pregnant mice had a partial placenta accreta phenotype. The HTR8/SVneo cell line was used as an in vitro model to elucidate the underlying mechanisms of MARVELD1-mediated trophoblast invasion. We detected a diminished expression of integrin β4 upon the downregulation of MARVELD1 and enhanced migration and invasive abilities of trophoblast cells both in vivo and in vitro. The integrin β4 rescue assay also supported the results. In conclusion, this study found that MARVELD1 mediated the invasion of trophoblast cells via regulating the expression of integrin β4.