Placenta - Maternal Decidua

Embryology - 16 Apr 2024        Expand to Translate
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Introduction

Anchoring Villi and Maternal Decidua

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

Disordered IL-33/ST2 activation in decidualizing stromal cells prolongs uterine receptivity in women with recurrent pregnancy loss "Decidualization renders the endometrium transiently receptive to an implanting blastocyst although the underlying mechanisms remain incompletely understood. Here we show that human endometrial stromal cells (HESCs) rapidly release IL-33, a key regulator of innate immune responses, upon decidualization. In parallel, differentiating HESCs upregulate the IL-33 transmembrane receptor ST2L and other pro-inflammatory mediators before mounting a profound anti-inflammatory response that includes downregulation of ST2L and increased expression of the soluble decoy receptor sST2. We demonstrate that HESCs secrete factors permissive of embryo implantation in mice only during the pro-inflammatory phase of the decidual process. IL-33 knockdown in undifferentiated HESCs was sufficient to abrogate this pro-inflammatory decidual response. Further, sequential activation of the IL-33/ST2L/sST2 axis was disordered in decidualizing HESCs from women with recurrent pregnancy loss. Signals from these cultures prolonged the implantation window but also caused subsequent pregnancy failure in mice. Thus, Il-33/ST2 activation in HESCS drives an autoinflammatory response that controls the temporal expression of receptivity genes. Failure to constrain this response predisposes to miscarriage by allowing out-of-phase implantation in an unsupportive uterine environment."

More recent papers

This table allows an automated computer search of the external PubMed database using the listed "Search term" text link. This search now requires a manual link as the original PubMed extension has been disabled. The displayed list of references do not reflect any editorial selection of material based on content or relevance. References also appear on this list based upon the date of the actual page viewing. References listed on the rest of the content page and the associated discussion page (listed under the publication year sub-headings) do include some editorial selection based upon both relevance and availability. 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.

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.

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)

Prokineticin 1

Prokineticin 1 (PROK1) signalling via prokineticin receptor 1 (PROKR1) regulates Dickkopf 1 (DKK1) expression, a negative regulator of canonical Wnt signaling.

References

Articles

<pubmed>21144801</pubmed>

Search PubMed

Search Pubmed: Maternal Decidua | Decidualization

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Cite this page: Hill, M.A. (2024, April 16) Embryology Placenta - Maternal Decidua. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Placenta_-_Maternal_Decidua

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© Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G