Positive regulation of placentation by L-amino acid transporter-1 (lat1) in pregnant mice

Abstract

Placenta plays multi-functions in embryo-uterine dialogue through facilitating gas and nutrient exchange, providing an immunological barrier between the fetus and mother and secreting hormones and growth factors to regulate pregnancy. The successful formation and development of placenta requires invasion and differentiation of trophoblast cells, and any defects would result pregnancy related diseases such as intrauterine growth retardation (IUGR), preeclampsia (PE). Lat1 (L-type amino acids transporter 1) is a major Na ⁺ independent transporter of large neutral amino acids, including several essential amino acids. It has been showed that amino acid was fundamental regulator on cell function and energy metabolism in early embryonic development. It has been reported that Lat1 mRNA expressed in zygote, blastocyst during the pre-implantation stages and trophoblast giant cells (TGCs) in post-implantation placenta in mouse. Little is known the role of lat1 on placentation. Our research was to explore the effects of lat1 on the placentation in mouse. The expression of lat1 was detected from day 9 to 18 of pregnancy in placenta. The effects of lat1 on placentation were assessed with inhibitor of leucine transport 2-aminobicyclo-(2, 2, 1)-haptane-2-carboxylic acid (BCH) treatment by uterine horns injection on day 8 (D8) of pregnancy. The protein of lat1 was mainly localized in the cytoplasm of maternal decidual cell, spongiotro-phoblast cell (Sp) and labyrinth (Lab). Inhibition of lat1 transportation activity by uterine horns injection with BCH in vivo results in disorder of placental anatomical structure in mid-late pregnancy. These results suggest that lat1 might play an important role in mouse placentation progress.