The DSCs-Expressed CD82 Controls the Invasiveness of Trophoblast Cells via Integrinbeta1/MAPK/MAPK3/1 Signaling Pathway: Conclusion

Trophoblast invasion involves protelysis and remodeling of the uterine decidua. In addition to the MMPs, the integrin repertoire of the endometrium and decidua may play an important role in successful implantation. According to a timed expression correlating with embryo attachment, the avp3 and a4p1 integrins are considered markers of uterine receptivity. The avp3 integrin has been shown to be highly expressed at the time of embryo attachment, and aberrant expression of avp3 is associated with infertility. The miscarriage has been found to have a lower expression of a4p3 and a5p1 integrins in the endometrium during the implantation window than that of unexplained infertility. Moreover, the trophectoderm also express several integrins, a3, a5, p1, p3, p4, and p5, that are implicated in blastocyst attachment to the endometrial surface. In female mice lacking a functional integrinp1 gene, embryos develop normally to the blastocyst stage but fail to implant properly and die. In our study, CD82 in DSCs down-regulates the expression of integrinp1, which suggests a mechanism of CD82 in DSCs that controls the invasiveness of trophoblast cells.
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Pregnancy is characterized by high levels of estrogen, progesterone, and hCG, which play important roles in theĀ implantation process. Human CG can stimulate trophoblast migration through IGF2 and MMP9. Progesterone may decrease invasion and gelatinase expression in trophoblast cells of the first trimester, but increase the invasion and MMP2 expression in trophoblast cells of the late pregnancy. We have demonstrated that hCG attenuates CD82 expression in DSCs, but estrogen or progesterone has no effect on the CD82 expression. So we conclude that hCG secreted by syncytio-trophoblastic cells might increase invasiveness of the extra-villous trophoblast cells through down-regulating the expression of CD82 in DSCs. As is well known, several studies have reported the expression of hCG in a variety of cancers, including trophoblastic and testicular germ cell tumors, bladder cancer, colorectal cancer, ovarian cancer, lung cancer, pancreatic cancer, cervical cancer, prostate cancer, and breast cancer. It is further reported that such cancers have poor prognosis and adverse survival rate. The role of hCG or its subunits with respect to the biology of the tumor cells is not fully clear. In view of our results, we presume that abnormal levels of hCG secreted by the cancer cells might promote their invasion and metastasis by down-regulating the expression of CD82.
Interestingly, we have found that the transcription and translation of CD82 in decidual tissues from unexplained miscarriage are significantly higher than that of the normal early pregnancy, which suggests that the CD82 overexpression at the maternal-fetal interface would lead to the early pregnancy wastage.
In summary, our study has demonstrated for the first time that CD82 expressed in DSCs participates in intercellular communication with trophoblast cells, which is different from our previous understanding that CD82 in tumor cells mainly inhibits the motility and invasion of itself. Further research may focus on the functional molecules and proteins that regulate the expression of CD82, such as the anti-hCG vaccine, which will help to potentially control both pathological trophoblastic disease and tumor.

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