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The depletion of MARVELD1 leads to murine placenta accreta via integrin β4‐dependent trophoblast cell invasion
Author(s) -
Chen Yue,
Zhang Hui,
Han Fang,
Yue Lei,
Qiao Chunxiao,
Zhang Yao,
Dou Peng,
Liu Weizhe,
Li Yu
Publication year - 2018
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.26098
Subject(s) - trophoblast , placenta , integrin , microbiology and biotechnology , placenta accreta , biology , in vitro , downregulation and upregulation , knockout mouse , andrology , cell adhesion , cell culture , cell , fetus , receptor , pregnancy , medicine , genetics , gene
The placenta is a remarkable organ, it serves as the interface between the mother and the fetus. Proper invasion of trophoblast cells 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 migrate 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 during placenta development.