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Functions of the Placenta

The placenta is a relatively under-studied organ. Only half of us humans (the XX half) have the ability to form placentas, and not all of those capable of making one actually do make one. So it is not part of the anatomy and physiology of all humans. However, for nine months, the placenta supports each of us, and it is an organ with several critically important functions.

These functions include: anatomical support, nutrient transfer, oxygen transfer and carbon dioxide exchange, endocrine support, and immune suppression. These functions are summarized in the website http://www.embryology.ch/anglais/fplacenta/planmodpl01.html, which is produced by the online course in embryology for medicine students developed by the universities of Fribourg, Lausanne, and Bern (Switzerland).

The support functions of the placenta have been outlined in Website 9.1.

Endocrine Functions

One of the critical functions of the placenta is to produce the steroid hormone progesterone. As its name implies, it is the hormone that allows the continuation of pregnancy. In humans, this hormone is initially made by the corpus luteum (of the ruptured ovarian follicle), but after the 4th month of pregnancy, it is mostly the progesterone made from the trophoblast that allows the maintenance of pregnancy. Progesterone prevents the uterine muscles from contracting and aids in the differentiation of the mammary glands that will produce the milk necessary for the infant.

During the initial stages of pregnancy, the corpus luteum is instructed to produce progesterone (and estrogen) by human chorionic gonadotropin (hCG) which is secreted by the syncytiotrophoblast portion of the placenta. This is the compound that is measured in pregnancy tests and is an excellent way to monitor early pregnancy.

Placental lactogen is also made by the syncytiotrophoblast (and the cytotrophoblast). It is an insulin-like peptide that acts to enhance fetal growth and at the same time, prepares the mammary gland for milk production.

Materno-Fetal Exchange of Nutrients and Gasses

The oxygen/carbon dioxide exchange in the placenta has been mentioned in the textbook and is mediated by hemoglobin. Fetal hemoglobin binds to oxygen more avidly than adult hemoglobin, so there is a net transfer of oxygen from the mother to the fetus. Carbon dioxide from the fetus will take up the site in the hemoglobin of the maternal blood, and it will be exhaled in the lungs.

Simple diffusion down concentration gradients is responsible for the transport of non-polar molecules and fat-dissolvable substances such as fats and alcohol. The dangers of alcohol to the nervous system of the fetus are discussed in Chapter 20.

Water, a strongly polarized molecule, cannot transverse the cell membrane. It crosses the placenta through specialized pores called the aquaporines that are formed by specialized proteins in the plasma membrane.

Active transport is critically important in getting nutrients into the fetus. Glucose is the major source of energy to the fetus. It is transported across the placenta by facilitated diffusion via hexose transporters. Although the fetus receives large quantities of glucose, much of it is oxidized within the placenta to lactic acid, which is used for fetal energy production.

Since the concentrations of some amino acids are higher in the fetal blood than in the maternal circulation, these amino acids need to be transported into the fetus by active transport mechanisms. At least 10 sodium-dependent amino acid transporters have been found in human placenta. There is also substantial metabolism of some amino acids as they cross the placenta.

Immune “Cloaking”

The placenta also provides a cloak against the mother’s immune system. It must be recalled that the fetal cells have proteins derived from the father’s genome and which can elicit an immune response from the mother. If grafted onto the mother, the father’s cells would be rejected. How is it that the fetus can survive nine months without being rejected?

Transplanted cells from a genetically distinct organism (as the fetus would be to the mother) are usually killed by the immune system. In humans, the recognition of “self” is regulated by histocompatibility proteins, HLA-A and HLA-B,on the cell membranes. If these are different, the lymphocytes of the immune system proliferate and attack them. If there is neither HLA-A nor HLA-B on the cell, another group of immune cells, the natural killer (NK) cells, destroy the graft. The trophoblastic part of the placenta contains the chromosomes of both the mother and the father, and it is the place where the maternal circulation can see fetal cells. In the trophoblast, the classical immune proteins, HLA-A and HLA-B, are down-regulated. Therefore, the mother’s lymphocytes will not mount an immune response. Moreover, the trophoblast produces a cell membrane protein called HLA-G. This protein is very much like HLA-A and HLA-B, and it resembles them closely enough to “fool” the NK cells. (In other words, the receptors on the NK cells bind to HLA-G and give the same signal as they would with HLA-A or HLA-B.) Therefore, the down-regulation of HLA-A and HLA-B gives protection from cytotoxic T-cells (the T-lymphocytes that mediate against grafts), while the presence of HLA-G (which looks similar to HLA-A and HLA-B and is recognized by natural killer cells as “self”) prevents the natural killer cells from attacking the fetus (Lash et al. 2010).

Another agent protecting the fetus is progesterone. Progesterone, among its many functions, also appears to prevent the lymphocytes from dividing around the fetus. As a result, the immune response, if initiated, cannot be maintained (Clements et al. 1979; Lee et al. 2012). Other agents may also prevent immune responses against the fetus; but the cessation of lymphocyte proliferation and the “cloaking” of the fetus, such that the immune system can’t see it as “non-self,” make being a eutherian mammal possible.

Literature Cited

Clemens, L., P. Siiteri and D. Stites. 1979. Mechanism of immunosuppression of progesterone on maternal lymphocyte activation during pregnancy. J. Immunol. 122: 1978–1985.

Lash, G., S. Robson and J. Bulmer. 2010. Review: Functional role of uterine natural killer (uNK) cells in human early pregnancy decidua. Placenta 31(S): 87–92.

Lee, J. H., J. P. Lydon and C. H. Kim. 2012. Progesterone suppresses the mTOR pathway and promotes generation of induced regulatory T cells with increased stability. Eur. J. Immunol. 42: 2683–2696.

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