Placenta - Maternal Decidua
Embryology - 26 Apr 2024 Expand to Translate |
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Introduction
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.
For the non-pregnant uterus background see Menstrual Cycle and Uterus Development.
Some Recent Findings
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More? References | Discussion Page | Journal Searches | 2019 References | 2020 References Search term: Maternal Decidua <pubmed limit=5>Maternal Decidua</pubmed> |
Maternal Decidua
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 parietalis.
These 3 regions are named by their positional relationship to the conceptus.
Maternal Immune
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 |
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Chemokine Gene Silencing
- Remove the attraction of maternal immune cells.
A mouse study[3] 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.
Corticotropin-Releasing Hormone
- 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).[4] (Note - This cannot be the only mechanism, as mice with dysfunctional FasL proteins are still fertile).
Decidualization Factors
Preimplantation factor
- 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.[5]
Activin A
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)[6]
Prokineticin 1
Prokineticin 1 (PROK1) signalling via prokineticin receptor 1 (PROKR1) regulates Dickkopf 1 (DKK1) expression, a negative regulator of canonical Wnt signaling.[7]
References
Reviews
Articles
<pubmed>21144801</pubmed>
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Search Pubmed: Maternal Decidua | Decidualization
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Cite this page: Hill, M.A. (2024, April 26) Embryology Placenta - Maternal Decidua. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Placenta_-_Maternal_Decidua
- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G