Placenta - Maternal Decidua

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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.

Placenta Links: placenta | Lecture - Placenta | Lecture Movie | Practical - Placenta | implantation | placental villi | trophoblast | maternal decidua | uterus | endocrine placenta | placental cord | placental membranes | placenta abnormalities | ectopic pregnancy | Stage 13 | Stage 22 | placenta histology | placenta vascular | blood vessel | cord stem cells | 2013 Meeting Presentation | Placenta Terms | Category:Placenta
Historic Embryology - Placenta 
1883 Embryonic Membranes | 1907 Development Atlas | 1909 | 1910 Textbook | 1917 Textbook | 1921 Textbook | 1921 Foetal Membranes |1921 human | 1921 Pig implantation | 1922 Single placental artery | 1923 Placenta Review | 1939 umbilical cord | 1943 human and monkey | 1944 chorionic villus and decidua parietalis | 1946 placenta ageing | 1960 monkey | 1972 Placental circulation | Historic Disclaimer

Some Recent Findings

  • Leukocyte driven-decidual angiogenesis in early pregnancy[1] "Successful pregnancy and long-term, post-natal maternal and offspring cardiac, vascular and metabolic health require key maternal cardiovascular adaptations over gestation. Within the pregnant decidualizing uterus, coordinated vascular, immunological and stromal cell changes occur. ...One of the earliest uterine responses to pregnancy in species with hemochorial placentation is stromal cell decidualization, which creates unique niches for angiogenesis and leukocyte recruitment. In early decidua basalis, the aspect of the implantation site that will cradle the developing placenta and provide the major blood vessels to support mature placental functions, leukocytes are greatly enriched and display specialized properties. UNK cells, the most abundant leukocyte subset in early decidua basalis, have angiogenic abilities and are essential for normal early decidual angiogenesis."
  • Disordered IL-33/ST2 activation in decidualizing stromal cells prolongs uterine receptivity in women with recurrent pregnancy loss[2] "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."
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Search term: Maternal Decidua

<pubmed limit=5>Maternal Decidua</pubmed>

Maternal Decidua

Placenta and Decidua[3]

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.

Human placenta SERPINE2 expression 02.jpg

Immunostained placenta and decidua. [3]

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.

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
  • Macrophages represent about 20% of all leukocytes.
  • regulatory role at the fetal-maternal interface.
  • M2 macrophage phenotype involved in tissue remodeling and inhibit inflammation
  • maintenance of tolerance to the non-self semi-allogeneic fetus
  • activated by fetal HLA-C (expressed on extravillous trophoblast cells)
  • specific immune tolerance to fetal alloantigens
  • Killer Inhibitory Receptor (KIR) activation by fetal HLA-C (expressed on extravillous trophoblast cells)

Chemokine Gene Silencing

Remove the attraction of maternal immune cells.

A mouse study[4] 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).[5] (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.[6]

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)[7]

Prokineticin 1

Prokineticin 1 (PROK1) signalling via prokineticin receptor 1 (PROKR1) regulates Dickkopf 1 (DKK1) expression, a negative regulator of canonical Wnt signaling.[8]


  1. <pubmed>25066422</pubmed>
  2. <pubmed>23300625</pubmed>| PLoS One.
  3. 3.0 3.1 <pubmed>21806836</pubmed>| Reprod. Biol. Endocrinol.
  4. <pubmed>22679098</pubmed>
  5. <pubmed>11590404</pubmed>
  6. <pubmed>20452489</pubmed>
  7. <pubmed>18434375</pubmed>
  8. <pubmed>21546446</pubmed>




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Cite this page: Hill, M.A. (2020, January 28) Embryology Placenta - Maternal Decidua. Retrieved from

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© Dr Mark Hill 2020, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G