Opa interacting protein 5 promotes proliferation and migration of trophoblast cells via activating STAT3 pathway.

Missed abortion, one of the leading causes of maternal and perinatal mortality, is associated with impaired trophoblast function. Opa interacting protein 5 (OIP5) interacts with outer membrane proteins, Opa, to play an important role in mitosis and tumorigenesis. The role of OIP5 in missed abortion was investigated in this study. Firstly, the expression of OIP5 in villous samples from patients with missed abortion was compared with women with normal pregnancies. Result showed that OIP5 was down-regulated in the placental villi from patients with missed abortion. Secondly, human first-trimester extravillous trophoblast-derived cell line (HTR-8/SVneo) was transfected with shRNA targeting OIP5 (shOIP5) or pcDNA-OIP5 (OIP5). Data from MTT and flow cytometry assays demonstrated that knockdown of OIP5 reduced number of viable cells in HTR-8/SVneo, and promoted the cell apoptosis. However, over-expression of OIP5 increased the number of viable cells and suppressed the cell apoptosis in HTR-8/SVneo. Moreover, cell migration of HTR-8/SVneo was inhibited by silencing of OIP5, and OIP5 over-expression enhanced protein expression of matrix metallopeptidase (MMP) 2/9. Lastly, OIP5 contributed to phosphorylation of STAT3 (signal transducer and activator of transcription 3) in HTR-8/SVneo. Inhibition of STAT3 attenuated OIP5 over-expression-induced increase in number of viable cells and migration in HTR-8/SVneo. In conclusion, OIP5 contributed to the proliferation and migration of trophoblast cell through activation of STAT3 signaling.