Search

Amino acids have an important role in the pre and post implantation of placenta and embryo development. l-type amino-acid transporter 1 (lat1) is responsible for the transportation of large neutral amino acids and is mainly expressed in human fetal liver, placenta, brain, etc. This study is the first to investigate the expression of lat1 in the early pregnancy of mouse uteri and its role in the process of decidualization. Endometrial stromal cells of a mouse model were used to evaluate decidualization from Day 4–8 of pregnancy in vitro followed by lat1 knock down by small interfering RNA and by a competitive inhibitor of Leucine transport 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH). The effects of lat1 on decidualization in vivo were assessed by injecting BCH into the uterine horns. The mRNA and protein expressions of lat1 in the implantation sites were higher than that in the inter-implantation sites and were localized in the luminal and gland epithelium, stromal and decidual cells. Its increased expression (p < 0.05) was associated with artificial decidualization as well as activation of prl expression. Down-regulation of lat1 expression in these cells by siRNA and BCH inhibited the decidual progression in vitro. Inhibition of lat1 transportation by BCH controlled decidual progression in vivo also accompanied the down-regulation of prl, lat1 expression in the decidual area and embryo size on Day 8 of pregnancy. In conclusion, these results revealed that lat1 might play an important role in the decidual progression both in vitro and in vivo.

Background Well-controlled trophoblast invasion at maternal-fetal interface is a critical event for the normal development of placenta. CD82 is a member of transmembrane 4 superfamily, which showed important role in inhibiting tumor cell invasion and migration. We surmised that CD82 are participates in trophoblast differentiation during placenta development. Methodology/Principal Findings CD82 was found to be strongly expressed in human first trimester placental villous and extravillous trophoblast cells as well as in trophoblast cell lines. To investigate whether CD82 plays a role in trophoblast invasion and migration, we further utilized human villous explants culture model on matrigel and invasion/migration assay of trophoblast cell line HTR8/SVneo. CD82 siRNA significantly promoted outgrowth of villous explants in vitro (P