A mother’s risk of getting preeclampsia, a potentially life-threatening illness associated with pregnancy, can be linked in some cases to genes from her foetus.

For the first time, a relationship has been found between foetal genes and the risk of preeclampsia in the mother.

Norwegian researchers, including a team from NTNU, figure prominently in the international group that presented the find in the journal Nature Genetics.

Preeclampsia affects around 3 per cent of births in Norway; worldwide, that number is estimated to be about 5 per cent.

In the vast majority of cases, the mother has mild symptoms, typically high blood pressure. Nevertheless, preeclampsia is one of the leading causes of death in both mothers and babies around the time of birth, and sometimes the only way to treat it is to deliver the baby, even prematurely.

“For the first time ever, we have discovered a foetal gene that increases the risk of preeclampsia,” says Ann-Charlotte Iversen at the Department of Cancer Research and Molecular Medicine at NTNU.

She says there has not been much research on the role of foetal genes in triggering the illness.

Preeclampsia usually begins with a problem in the placenta, which is mainly composed of foetal cells.For that reason, it makes sense that foetal cells might have a hand in causing the illness, Iversen said, even though it is the mother’s symptoms during the last part of the pregnancy that lead to the diagnosis.

“Our findings are particularly solid for three reasons: we analysed a large number of individuals, we found several genetic variables that all point to the same gene associated with the risk, and two independent population studies confirmed that this gene is associated with the risk,” Iversen said.

There are also a number of major studies that support the conclusions. CEMIR is one of 12 partners from 6 different countries in an EU project called InterPregGen, which was created in 2011.

“We are all working together to uncover the genetic risk factors for preeclampsia in the mother and foetus. We have linked a number of major European population studies to conduct the world’s largest genetic study of preeclampsia,” says Iversen. “Our contribution to the project has been information on a group of women from the HUNT study who have had problematic and healthy pregnancies, as well as information from the Preeclampsia Biobank, which has been collected independently.”

The genetic variants identified by the researchers are associated with the FLT-1 gene, which encodes a protein that in soluble form is known as a biomarker for preeclampsia.

The protein contributes to damaging the mother’s vascular system so that she develops symptoms such as high blood pressure and an increased amount of protein in the urine. This happens as a result of problems with the placenta, essentially because foetal cells in the placenta produce the protein.

“We have shown here that the risk of disease may be because changes in the gene affect how the protein works and how it affects the mother. This is a foetal gene that gives the mother an increased risk of developing preeclampsia. This find clearly brings us closer to a better understanding of preeclampsia,” Iversen said.