Regulation of Human Trophoblast GLUT3 Glucose Transporter by Mammalian Target of Rapamycin Signaling

摘要: Glucose transporter isoform-3 (GLUT3), one of the primary placental facilitative glucose transporters responsible for basal transport, has a crucial role in transport and fetal growth during early pregnancy. A GLUT3 mutation mice been reported to cause loss pregnancy or late-gestational restriction. However, underlying mechanisms that regulate humans are largely unknown. In present study, we used JEG-3 human choriocarcinoma cell line, which resembles first trimester model, study mammalian target rapamycin complex 1 (mTORC1) regulation GLUT3. We combined treatment small interfering (si) RNA-mediated silencing approaches with mRNA protein expression/localization studies investigate alteration expression localization following mTORC1 inhibition trophoblasts. Inhibition signaling by raptor decreased (−41%) (−50%). Similar effects were obtained cells was inhibited rapamycin. Immunofluorescence analysis revealed markedly reduced surface cytoplasm response silencing. Because activity intrauterine restriction, our data suggested possible mechanism abnormal this complication.