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Updated: Aug 8, 2026

Isolation of Leukocytes from the Human Maternal-fetal Interface
Published on: May 21, 2015
Leukemia inhibitory factor produced at the fetomaternal interface stimulates chorionic gonadotropin production: its
K Sawai1, N Matsuzaki, T Kameda
1Department of Obstetrics and Gynecology, Osaka University Medical School, Japan.
Insights
Leukemia inhibitory factor (LIF) stimulates trophoblasts to produce chorionic gonadotropin (CG), crucial for placental function and embryo growth. This process involves the glycoprotein 130 (gp130) receptor and tyrosine kinase signaling.
Area of Science:
- Reproductive biology
- Endocrinology
- Cell signaling
Background:
- Leukemia inhibitory factor (LIF) and interleukin-6 (IL-6) are cytokines present at the fetomaternal interface.
- The role of LIF in early human embryo implantation and placental development requires further elucidation.
- Glycoprotein 130 (gp130) is a shared receptor component for both LIF and IL-6.
Purpose of the Study:
- To investigate the role of leukemia inhibitory factor (LIF) in human embryo implantation.
- To determine the involvement of gp130 and tyrosine kinase signaling in LIF-mediated trophoblast functions.
- To assess the production of chorionic gonadotropin (CG) in response to LIF and IL-6.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) to quantify LIF and IL-6 levels in decidual and chorionic tissues.
- Reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry to detect gp130 expression and localization.
- In vitro stimulation of trophoblasts with recombinant LIF (rLIF) and recombinant IL-6 (rIL-6), with or without blocking antibodies (anti-gp130, anti-IL-6 receptor) and genistein.
Main Results:
- Decidual tissue produced higher LIF levels than chorionic tissue, while IL-6 was higher in chorion.
- Trophoblasts expressed gp130, the shared receptor for LIF and IL-6.
- Recombinant LIF (rLIF) induced chorionic gonadotropin (CG) production similar to rIL-6.
- LIF-induced CG production was blocked by anti-gp130 antibody, indicating gp130 mediation.
- Both LIF- and IL-6-induced CG production were blocked by genistein, suggesting tyrosine kinase involvement.
Conclusions:
- LIF produced at the fetomaternal interface stimulates trophoblasts to produce CG via gp130 and tyrosine kinase signaling.
- LIF plays a significant role in maintaining placental functions and supporting embryonal growth through CG production.
- These findings highlight LIF as a key factor in early pregnancy maintenance.
Abstract:
We investigated the role of leukemia inhibitory factor (LIF) at the implantation site of human embryos. The first trimester decidual tissue produced higher levels of LIF than chorionic tissue, but the decidua produced much smaller amounts of interleukin-6 (IL-6) than the chorion in vitro, as determined by enzyme-linked immunosorbent assay. The reverse transcription-polymerase chain reaction and immunohistochemical analysis revealed the expression and localization, on the trophoblasts, of glycoprotein 130 (gp130), an IL-6 signal transducer receptor component shared by the cytokines such as LIF and IL-6. Trophoblasts stimulated by recombinant LIF (rLIF) produced CG titer at the amount similar to that induced by rIL-6. Recombinant LIF-induced CG production was significantly blocked by anti-gp130 antibody but not by anti-IL-6 receptor antibody, whereas rIL-6-induced CG was completely blocked by both antibodies. Recombinant LIF- and rIL-6-induced CG productions were both significantly blocked by genistein, a tyrosine kinase inhibitor, suggesting an involvement of tyrosine kinase in gp130-mediated CG production. Since CG is capable of stimulating trophoblast growth and differentiation as well as placental metabolism, LIF produced at the fetomaternal interface are considered to stimulate the trophoblasts to produce CG, which may contribute to the maintenance of the placental functions and embryonal growth.
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