Placenta - Maternal Decidua
|Embryology - 20 Oct 2019 Expand to Translate|
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- 1 Introduction
- 2 Some Recent Findings
- 3 Maternal Decidua
- 4 Maternal Immune
- 5 Decidualization Factors
- 6 References
- 7 Glossary Links
This page gives an overview of aspects of maternal component of placental development, formed initially by the decidualization of the endometrium.
In week 2, the trophoblast shell cells proliferate and form a syncitiotrophoblast and cytotrophoblast layer around the conceptus. Syncitiotrophoblast cells migrate into the uterine wall, forming maternal blood-filled spaces (lacunae).
Decidualization is the process of converting endometrial stromal cells into decidual cells and requires at least 8–10 days of hormone stimulation. A similar "decidual" cellular change, but less significant, also occurs in the uterine lining after ovulation during the secretory phase of the non-pregnant uterus.
- initiated during the mid-secretory phase of the menstrual cycle
- in response to elevated progesterone levels
- acts mainly through progesterone receptor (PR) PR-A (other isoform is PR-B)
Placentation begins once the conceptus begins to implant in the uterine wall and the placenta will have both a fetal and a maternal component.
During pregnancy, both the maternal blood volume increases by about 50% and the uterine blood flow increases 10 to 12 fold. Flow increase is due to the trophoblast cell invasion of the spiral arteries opening them into blood-filled spaces of the placenta.
Some Recent Findings
|More recent papers|
This table allows an automated computer search of the external PubMed database using the listed "Search term" text link.
Search term: Maternal Decidua
<pubmed limit=5>Maternal Decidua</pubmed>
The maternal uterine endometrium stromal cells (fibroblast-like) are transformed by steroid hormones (progesterone) and embryonic signals into the decidua.
The entire maternal decidua is divided into three regions: decidua basalis, decidua capsularis and decidua parietals (decidua vera).
These 3 regions are named by their positional relationship to the conceptus.
Immunostained placenta and decidua. 
SERPINE2 was extensively detected in decidual cells (dc), cytotrophoblasts, extravillous trophoblasts at the junction zone of the cell column (cc) and anchoring villi (av), and the endothelia of the spiral artery (sa); and weak staining was found in fibrinoids (f) and the villous mesenchyme.
How does the implanting conceptus avoid immune rejection by the maternal immune system? There are a number of maternal and embryonic mechanisms that are thought to act to prevent immune rejection of the implanting conceptus, though the complete mechanism(s) are unknown. This is particularly relevant to Assisted Reproductive Technologies involving donor eggs.
Below are some examples of research on this topic.
Decidual Immune Cells
- Specialised immune cells.
|Decidual Macrophages (Mϕ)||Decidual T cells||Uterine Natural Killer cells|
Chemokine Gene Silencing
- Remove the attraction of maternal immune cells.
A mouse study has shown that the normal immune response to inflammation, accumulation of effector T cells in response to chemokine secretion does not occur during implantation. This is prevented locally by epigenetic silencing of chemokine expression in the decidual stromal cells.
- Kill the maternal immune cells.
Both maternal and implanting conceptus release CRH at the embryo implantation site. This hormone then binds to receptors on the surface of trophoblast (extravillous trophoblast) cells leading to expression of a protein (Fas ligand, FasL) that activates the extrinsic cell death pathway on any local maternal immune cells ( T and B lymphocytes, natural killer cells, monocytes and macrophages). (Note - This cannot be the only mechanism, as mice with dysfunctional FasL proteins are still fertile).
There are a number of known molecular signals involved in the conversion of uterine stromal cells into decimal cells.
- Preimplantation factor (PIF) secreted only by viable embryos.
- a 15 amino acid peptide MVRIKPGSANKPSDD
- regulates immunity, promoting embryo-decidual adhesion, and regulating adaptive apoptotic processes.
Member of the a transforming growth factor beta (TGFbeta) superfamily, contributes to human endometrial stromal cells (HESC) decidualization and has been localized to decidual cells in the human endometrium. (possibly also BMP2 and TGFbeta1)
Prokineticin 1 (PROK1) signalling via prokineticin receptor 1 (PROKR1) regulates Dickkopf 1 (DKK1) expression, a negative regulator of canonical Wnt signaling.
Macrophage Inhibitory Cytokine
Macrophage inhibitory cytokine (MIC-1) inhibits trophoblast invasion by blocking activation of MMP-2 and -9.
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Cite this page: Hill, M.A. (2019, October 20) Embryology Placenta - Maternal Decidua. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Placenta_-_Maternal_Decidua
- © Dr Mark Hill 2019, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G