Gonadotropin-Releasing Hormone Type II (GnRH-II) Agonist Regulates the Motility of Human Decidual Endometrial Stromal Cells: Possible Effect on Embryo Implantation and Pregnancy1
33
Citation
47
Reference
10
Related Paper
Citation Trend
Abstract:
Invasion of the maternal decidua by extravillous trophoblast is an important process for embryo implantation and placentation in humans. Motile behavior of decidual endometrial stromal cells has been considered of critical importance for embryo implantation and programming of human pregnancy. The gonadotropin-releasing hormone (GnRH) effects in endometrium have raised concerns in reproduction. In the present study, we examined the action of GnRH-II agonist-promoted motility of human decidual endometrial stromal cells and the mechanisms of the action, indicating the role of GnRH-II agonist in embryo implantation and early pregnancy. Human decidual endometrial stromal cells were isolated from the decidual tissue from healthy women undergoing elective pregnancy termination of a normal pregnancy at 6- to 12-wk gestation, after informed consent. Cell motility was estimated by invasion and migration assay. Zymography and immunoblot analysis were performed to investigate the mechanisms of the GnRH-II action. The GnRH-I receptor (GnRH-IR) was expressed in human decidual tissue and endometrial stromal cells. The GnRH-II agonist promoted cell motility. Mitogen-activated protein kinase inhibitors abolished GnRH-II agonist-induced cell motility and activation of MMP-2 and MMP-9. GnRH-II agonist-mediated cell motility was suppressed by knockdown of endogenous GnRH-IR, MMP (matrix metalloproteinase)-2, and MMP-9 with small interfering RNA and MMP inhibitors. Our study demonstrates that the GnRH-II agonist promoted the cell motility of human decidual endometrial stromal cells through the GnRH-IR and the phosphorylation of extracellular signal-regulated protein kinase 1/2 and JNK-dependent activation of MMP-2 and MMP-9. Our findings represent a new concept regarding the mechanisms of GnRH-II-promoted cell motility, suggesting that GnRH-II agonist has strong effects on embryo implantation and decidual programming of human pregnancy.Keywords:
Decidual cells
Decidua
Trophoblast
Recent evidence of growth hormone (GH) receptor expression in rat endometrium and human myometrium have focused our attention on the role of the GH in endometrial development. We tested the expression of GH in the human endometrium throughout the menstrual cycle and during pregnancy.Immunohistochemical study was performed on endometrial specimens of fertile women in different periods of the menstrual cycle and in decidua of pregnant women.Glandular cells of the human endometrium were positive for GH in the mid and late luteal phase. Furthermore, the glandular cells of decidua showed intense staining for GH, while the stromal cells were negative. No immunostaining was expressed in the proliferative or early luteal phase. The intensity levels of staining for GH in decidual specimens were significantly higher than in glandular cells of secretory endometrium specimens (P < 0.01).The glandular cells of the human endometrium express GH from the late luteal phase throughout pregnancy in the decidual tissue. We suppose that GH plays an important role in blastocyst implantation.
Decidua
Decidualization
Immunostaining
Decidual cells
Myometrium
Cite
Citations (37)
Decidua
Trophoblast
Second trimester
Cite
Citations (12)
This chapter provides a general overview of the two major components of pregnancy-associated spiral artery remodeling, the maternal (decidual) and the fetal (trophoblastic). During placentation the mother comes in close contact with semi-allogeneic fetal trophoblastic cells which play a key role in maternal-fetal physiological exchange. Focusing on spiral artery invasion, there is little direct evidence for the occurrence of intrinsic trophoblastic defects in early pregnancy. Impaired trophoblast invasion in spiral arteries may not only be due to an intrinsic defect in invasive properties, but may also be induced by maternal cells. For a long time trophoblast invasion was thought to be controlled by a restrictive action of the decidua. A stimulatory role of decidua for trophoblast invasion may also apply to the endovascular invasion of the spiral arteries. Decidua-associated vascular remodeling not only occurs in the decidua but also in the junctional zone myometrial compartment.
Trophoblast
Decidua
Spiral artery
Placentation
Cite
Citations (30)
Decidua
Trophoblast
Placentation
Spiral artery
Myometrium
Placenta Accreta
Cytotrophoblast
Cite
Citations (27)
PROBLEM: The immunologic privilege afforded the fetus relies upon immunoregulation within the maternal‐fetal interface. Trophoblast and decidua‐derived immunoregulatory factors enforce this privilege by locally suppressing maternal responses to trophoblast antigens. The relative contribution of trophoblast or decidua immunosuppressive factors to pregnancy immunotolerance are not well characterized. The purpose of this study was to compare the suppressive effects of hydatidiform mole trophoblast and decidua extracts on interleukin‐2‐dependent proliferation. METHOD: Tissue extracts were prepared from hydatidiform mole trophoblast and decidua following uterine evacuation. Samples were submitted to interleukin‐2‐dependent and ‐independent cell proliferation assays. RESULTS: Hydatidiform mole trophoblast extract significantly ( P < 0.05) suppressed interleukin‐2‐dependent proliferation but did not affect interleukin‐2‐independent cell proliferation. In contrast, molar decidua extract suppressed both cell lines. CONCLUSIONS: Human hydatidiform mole trophoblast contains factor(s) that specifically abrogate interleukin‐2‐dependent clonal expansion of murine cytotoxic T‐cells. In contrast, extracts of molar decidua suppressed both interleukin‐2‐dependent and ‐independent responses. This indicates that the trophoblast antagonizes critical interleukin‐2‐mediated immunologic responses, but that the decidua uses nonspecific antiproliferative mechanisms for immunoregulation.
Decidua
Trophoblast
Cite
Citations (4)
Trophoblast
Decidua
Decidual cells
Placentation
Cite
Citations (51)
Summary. Mouse trophoblast and decidua were examined by means of immunohistochemistry to define the localization of type I interferon. The decidua were stained for type I interferon at the time of implantation. The strong reaction was first observed in the primary decidual zone on day 5 and subsequently in the secondary decidual zone on day 6. After day 10, the decidua basalis and decidua capsularis showed a strong reaction. At the one-cell stage, embryos were weakly labelled, but a positive reaction was recognized in compacted morulae. Blastocysts on days 3 and 4 were positive in trophoblast and inner cell mass and a strong reaction was observed in the primitive endoderm on day 4. The visceral endoderm on day 5 and the trophoblast on day 6 were positive. After day 10, the trophoblast giant cells, labyrinth, visceral yolk sac and fetal blood cells gave a positive reaction. This study is the first demonstration of type I interferon localization in situ in mouse trophoblast and decidua during decidual formation. Keywords: type I interferon; implantation; decidualization; trophoblast; mouse
Decidua
Trophoblast
Decidual cells
Interferon type I
Cite
Citations (15)
By observing the morphological changes of the human trophoblast and decidua cells as well as the HCG secretion by the trophoblast cells in vitro, we tried to elucidate the cytological mechanism of the anti- early pregnancy effect of α-momorcharin.The results showed that the treated trophoblast cells all had obvious morphological damage in different degrees after 24 h treatment with different concentrations of a-momorcharin (0.13, 0.50, 2.00 and 8.00μg / ml). The degrees of damage were dependent on the concentration and duration, and α-momorcharin showed an inhibitory effect on HCG secretion. The reduction of HCG secretion could be detected as early as6 h after the treatment and the cells almost lost their ability of secreting HCG after 24 h treatment. The decidua cells were also damaged by a-momorcharin, but they were not as sensitive as trophoblast cells.Our results proved that the a-momorcharin treatment could not only directly kill trophoblast cells, but also damage decidua cells. Therefore the α-momorcharin treatment can terminate early pregnancy.
Trophoblast
Decidua
Cite
Citations (0)
Cytotrophoblast
Decidua
Trophoblast
Decidual cells
Cite
Citations (6)