Abstract
During the process of placental development, syncytialization leads to structural and functional maturation of the placenta, and then placenta can exchange gas and nutrients between fetus and mother and produce placental hormones necessary for pregnancy maintenance. Several amino acid transporters are known to contribute to placental syncytialization, and inhibiting their expression could suppress the progression of syncytialization. In this regard, our previous study showed that valproic acid, which can cause congenital abnormalities, reduced the expression of SLC6A19, encoding the neutral amino acid transporter B0AT1, in the Human choriocarcinoma cell line BeWo. However, the involvement of SLC6A19 in placental syncytialization has not been cleared. Here, we tried to clarify the role of SLC6A19 in placental syncytialization. BeWo, which was knocked down SLC6A19 by shRNA, was treated with forskolin to induce syncytization, and the expression level of human chorionic gonadotropin β (hCGβ, gene; CGB) was analyzed by real-time RT-PCR. CGB expression was significantly reduced in cells knocked down SLC6A19 compared to control cells. Moreover, immunohistochemical staining showed that the ratio of hCGβ-positive cells in SLC6A19 knockdown BeWo cells was decreased relative to control cells. These results suggest that SLC6A19 might be involved in placental syncytialization. Now, to reveal its mechanism, we investigate the relationship between SLC6A19 suppression and the cAMP/PKA signaling pathway, which is important for placental syncytialization.
