Some congenital heart defects are linked to problems with the growth of the placenta, caused by alterations in protein levels.
- Congenital heart defects affect the heart and the blood vessels around it.
- According to a recent study, defects in the placenta may explain their appearance.
- These placental growth problems are linked to a protein, which has become a potential treatment avenue.
Congenital heart defects affect five out of 1,000 births according to the French Federation of Cardiology. They affect the heart or the blood vessels surrounding it. For many years, researchers have wanted to understand the causes of these malformations in order to reduce their risk of occurrence. In the specialist journal Developmentscientists from Nanjing University, China, explain that they have discovered one of the potential causes: the placenta.
What is the connection between the placenta and congenital heart defects?
“Previous research had suggested that some heart defects could be triggered by problems with the placenta, the organ that supplies oxygen and nutrients to the developing embryo.they specify in the preamble to their work. To better understand the link between the placenta and congenital heart defects, they carried out tests on mice. They were interested in a protein, SLC25A1, whose levels are reduced in certain patients with congenital heart defects. According to them, sheplays a key role in the transport of citric acid, an important metabolite whose derivatives can affect gene expression, to different regions of our cells.”. They therefore disrupted this protein in the tissues of mouse embryos. They found that loss of SLC25A1 does not directly affect the developing heart. “Instead, it leads to problems with placental growth and this, in turn, causes heart defects in mice.”they conclude.
Congenital heart defect: the specific role of a protein in the placenta
Their study took place in several stages. For the first, they used gene editing tools to produce mouse embryos that completely lack the SLC25A1 protein. These embryos developed heart defects and their placentas, which were thinner than usual. Then they removed the protein from parts of the embryo to understand where it was needed. In mouse embryos, they removed it from the forming heart. “Surprisingly, these mice did not develop heart defects, suggesting that SLC25A1 does not play an important role in heart cells.”they observe. Then, they generated mice that lacked the SLC25A1 protein in their placental tissue; they found that the animals developed both placental defects and heart defects.
A potential treatment for congenital heart defects?
Continuing their work, the Chinese scientists noticed that placentas lacking SLC25A1 had low levels of PSG1, a protein produced by placental cells. It is known to help regulate the development of the endothelium, a layer of cells that line the inside of certain body structures, including blood vessels. “We showed that administration of human PSG1 to pregnant mice reduces placental and cardiac malformations in embryos lacking SLC25A1explains Professor Zhongzhou Yang, director of the study. PSG1 could therefore become a potentially effective drug to help improve placental and cardiac development of the fetus in the womb.“
