胎儿生长受限（FGR）是妊娠期的严重并发症之一，胎盘细胞增殖减少、过度凋亡是导致FGR发病的重要原因。母亲孕期暴露全氟辛烷磺酸盐（PFOS）可导致FGR，但机制尚未明确。近年研究发现，长链非编码RNA（lncRNA）MEG3在胎盘及胚胎生长发育过程中发挥重要的作用。我们的前期研究结果提示PFOS可能通过上调lncRNA-MEG3及其内含子miR-770-5p而抑制靶基因STEAP4表达，进而引起胎盘细胞增殖、凋亡异常，导致FGR的发生。本项目拟结合动物及细胞实验，综合应用分子生物学、表观遗传学、生物信息学等研究手段，系统研究孕期PFOS暴露对胎盘及胚胎发育的影响，阐明lncRNA-MEG3/miR-770-5p/STEAP4通路在PFOS致FGR效应中的作用与机制。本研究可为FGR的发生机制提供新的理论依据，也为FGR的临床防治、提高人口质量作出贡献。

Fetal growth restriction (FGR) is one of the most significant complications in the perinatal period, and placental insufficiency of structure and function represents the cause of FGR. Studies have suggested that PFOS exposure may cause FGR; however, the mechanism remains to be elaborated. Accumulating evidences have demonstrated that the long non-coding RNA (lncRNA) MEG3 has received growing attention of the roles in the development of placenta and embryo. According to our previous studies, we have proposed that PFOS may induce unbalanced proliferation and apoptosis of placental trophoblasts cells through enhancing lncRNA-MEG3 and its intronic miR-770-5p, suppressing the target gene STEAP4, and then lead to the occurrence of FGR. In this project, we will apply the methods of molecular biology, epigenetics, bioinformatics, and systematically access the effect of PFOS on placental and embryonic development, clarify the role and mechanism of lncRNA-MEG3/miR-770-5p/STEAP4 signaling pathway in the occurrence of FGR in vivo and in vitro. This project will provide not only new theoretical evidence for the mechanisms of FGR, but also make contributions to improve the prevention and treatment of FGR, and the quality of the population health.