THE fetus receives food through the blood vessels of the placenta, a specialized organ that contains both baby and mother cells. As it grows, its nutritional demand is greater.
Between 10 and 15% of babies have low growth in the uterus, often due to less development of the placental vasculature. In humans, these blood vessels expand dramatically between the middle and the end of the gestation, when they reach a total length of approximately 320 kilometers.
Very large or very small babies are more likely to suffer or even die at birth and are at increased risk of developing diabetes and heart problems later in life
In a study published today in development cell, a team led by scientists from the Cambridge University (UK) used genetically modified mice to show how the fetus produces a signal that encourages blood vessel growth inside the placenta. This signal also causes changes in other placental cells to allow more nutrients from mother to baby.
“As it grows, the fetus needs the mother’s nourishment; and healthy blood vessels in the placenta are essential to get the right amount of nutrients you need,” he explains. Ionel Sandovici, first author of the work.
“We identified one of the ways the fetus uses to communicate with the placenta and cause the correct expansion of these blood vessels. When this communication is interrupted, the blood vessels do not develop properly and the baby will have difficulty getting all the food he needs”, adds the researcher.
IGF2 Hormone and Baby Growth
The scientific team found that the fetus sends a signal known as IGF2 –A peptide hormone involved in the regulation of cell proliferation, growth, migration, differentiation and survival– that reaches the placenta through the the umbilical cord.
In humans, IGF2 levels progressively increase after 29 weeks of gestation: a large contribution is associated with overgrowth and an insufficient amount with poor growth
In humans, IGF2 levels progressively increase between 29 weeks’ gestation and term: a large supply of IGF2 is associated with overgrowth, while an insufficient amount of IGF2 is associated with undergrowth.
Very large or very small babies are more likely to suffer or even die at birth and are at greater risk of developing diabetes and heart problems in adulthood.
“We have known for a long time that IGF2 favors the growth of the organs where it is produced. In this study, we showed that IGF2 acts as a classic hormone: it is produced by the fetus, passes into the fetal blood and, through the umbilical cord, to the placenta, where it acts”, adds the scientist.
Battle of the sexes in the genome
In mice, the response to IGF2 in placental blood vessels is mediated by another protein, called IGF2R. The two genes that make IGF2 and IGF2R are imprinted genes, that is, they are expressed in a specific way according to the father’s sex. In this case, only the copy of the IGF2 gene inherited from the father and the IGF2R gene inherited from the mother are active.
“One theory about imprinted genes is that genes expressed by the father are ‘greedy and selfish.’ They want to extract as much resources as possible from the mother. But the genes expressed by the mother act as a counterbalance to these demands”, he reveals. Michael Constance, co-author of the study.
The father’s gene stimulates the fetus’ needs for bigger blood vessels and more nutrients, while the mother’s gene in the placenta tries to control the amount of food it provides.
Miguel Constância, co-author of the study

“The father’s gene stimulates the fetus’ needs for bigger blood vessels and more nutrients, while the mother’s gene in the placenta tries to control the amount of food it provides. There is a tug of war, a battle of the sexes on a scale of genome”, Emphasizes the expert.
The team says their findings will provide a better understanding of how the baby, placenta and mother communicate during pregnancy. This, in turn, could lead to ways to measure fetal IGF2 levels and find ways to use drugs to normalize these levels or promote normal development of the placental vasculature.
Reference:
Sandovici et al. “The imprinted Igf2-Igf2r axis is critical for combining placental microvasculature expansion with fetal growth.” development cell; January 10, 2022: DOI: 10.1016 / j.devcel.2021.12.005
Source: SYNC
Rights: Creative Commons.
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