SYNCYTIOTROPHOBLAST: CHARACTERISTICS, FUNCTION, PLACENTAL APOPTOSIS - BIOLOGY - 2025

The syncytiotrophoblast is a multinucleated cytoplasmic mass that forms the outer layer of the trophoblast and contacts maternal tissue. This cell layer is found invading the epithelium and stroma of the endometrium during embryonic development of mammals. The cells that make up the syncytiotrophoblast fuse with each other, losing their cell membranes.

This layer of cells originates from the cell differentiation of the cytotrophoblast and is responsible for the exchange of gases and nutrients between the mother and the fetus. In addition, it is capable of producing hormones and peptides in the implantation phase of the blastocyst to the endometrium and the formation of the placenta.

Source: Henry Vandyke Carter

characteristics

As its name implies, the syncytiotrophoblast cells have lost their membranes and fused, giving this cell layer a multinucleated syncytial-like appearance.

These cells continuously cover the chorionic villous surface, the decidua basalis and the chorionic plate and form part of the placental barrier that is responsible for separating the mother's and fetal blood.

The syncytiotrophoblast arises from the proliferation and fusion of cytotrophoblast cells. The cells of this layer do not have proliferative capacity, that is, they do not undergo mitosis, so the expansion and maintenance of this cell layer depends only on the continuous incorporation of cells from the cytotrophoblast, ensuring its functionality.

These cells have Golgi complexes and abundant smooth and rough endoplasmic reticulum, and they also have a large number of mitochondria and lipid inclusions.

This cell layer also has a secretory function, releasing progesterone, estrogen, human chorionic gonadotropin (hCG) and lactogens. As cellular material ages, it is wrapped in a protective membrane and disposed of through the maternal circulation.

Role in embryonic development

Nidation or implantation

The blastocyst joins the endometrium initiating a stage of rapid cell proliferation, with the differentiation of the trophoblast into cytotrophoblast and syncytiotrophoblast. The latter extends through the endometrial epithelium until it reaches its stroma, where the cells fill with lipids and glycogen, turning into decidual cells.

These decidual cells undergo degenerative processes that allow them to provide nutrients to the developing embryo.

Once the blastocyst is implanted in the endometrium by the implantation or nesting process, the fusion of the outermost cells of the trophoblast, give rise to the primitive syncytiotrophoblast.

Later, lagoons are formed, occupied by glandular secretions of the endometrium, which will later be replaced by maternal blood, by weakening the capillaries and endometrial venules.

These intracellular gaps filled with maternal blood define the lacunar or trabecular phase and spread until they reach the opposite side of the implantation site.

The gaps in the syncytiotrophoblast are called trabeculae. Embryogenesis, which consists of changes in the embryoblast inside the blastocyst, also occurs at this stage.

Utero-placental circulation

One of the fundamental functions of the syncytiotrophoblast is the metabolic exchange between the mother and the fetus, demonstrating a high endocrine activity and participating in the homeostasis of embryonic development.

The appearance of intracellular or trophoblastic gaps in the syncytiotrophoblast initiates the development of the utero-placental circulation. Sinusoids derived from the capillaries of the maternal portion of the placenta flow into these lagoons.

A directional flow is formed by the differential pressure between the circulatory vessels and the trophoblastic lagoons. This flow goes from the arteries to the veins, forming the primitive utero-placental circulation.

There is a transfer of nutrients from the maternal vessels to the embryo, which is evident when observing the abundant pinocytic vesicles of the syncytiotrophoblast.

The syncytial cell layer lines the floating villi of the placenta. These villi come into contact with maternal blood when the utero-placental circulation is established, thus regulating the transport of oxygen and nutrients.

Placental apoptosis

Apoptosis or programmed cell death turns out to be an important component in embryonic development, thus the elimination of selected cells occurs, to prevent the indiscriminate loss of cells. Syncytial fusion of cytotrophoblast cells is the initial phase of the apoptotic cascade.

In the initial stage of apoptosis, cytotrophoblast cells proliferate and fuse to form the syncytial layer or syncytiotrophoblast.

In the execution phase of apoptosis, the cytoplasmic and nucleic material of the cytotrophoblast has passed into the syncytial layer, so that the cells of this last layer are equipped with the material necessary for the apoptotic cascade to start.

The apoptotic process presents a temporary pause due to the action of antiapoptotic enzymes, however, the caspase 3 enzyme reactivates this process, as it in turn activates components that degrade proteins and nucleic acids in cells. Other enzymes responsible for degrading cellular microfilaments are activated.

After the degradation of the cellular components, the waste is packaged in the apical membranes of the syncytiotrophoblast, originating the syncytial or apoptotic nodes, which will be finally released into the mother's bloodstream.

Apoptosis and preeclampsia

Preeclampsia is a pathology presented during pregnancy. Some investigations have shown that this pathology is caused by an alteration in the differentiation of the trophoblast due to an excess of apoptotic processes at this level.

The release of apoptotic wastes into the maternal bloodstream does not provoke inflammatory responses in the mother because these wastes are protected by a membrane that prevents them from coming into contact with maternal structures. The debris coating process takes a few weeks.

In preeclampsia, there is an excess proliferation and fusion of cytotrophoblast cells, which causes an increase in cellular degradation in the syncytiotrophoblast. This increase causes an accumulation of cellular debris, and a delay in the formation of their protective membrane.

This causes partially degraded debris and microfragments, including syncytiotrophoblast enzymes, to enter the mother's bloodstream, causing tissue damage. In addition to preeclampsia, hypoxic states in the placenta have been associated with an increase in cell apoptosis.

Evidence for the relationship between apoptosis and preeclampsia

Significant cytoplasmic concentrations of microfragments of the syncytiotrophoblast have been found in preeclamptic patients. These microfragments can alter the behavior of macrophages, causing both an increase in neutrophil activation and a decrease in endothelial relaxation.

These alterations in maternal blood cells explain the systemic damage and the manifestation of pre-eclampsia, which causes epithelial damage and an inflammatory response. In addition to causing damage to the placenta due to an increase in fibrinoid deposits on the villi.

References

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