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Genetic variation in progesterone receptor tied to prematurity risk | News Center

Genetic variation in progesterone receptor tied to prematurity risk | News Center

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Progesterone is also used as a medication for pregnant women at risk of delivering too early, such as those who have given birth prematurely before. Still, giving extra progesterone to such women does not always prevent an early delivery. No one knows why.

The new study used data from the 1,000 Genomes Project, a publicly accessible database of complete human genomes from people of different ancestral backgrounds. The researchers compared genetic sequences for the progesterone receptor in three populations: Utah residents with European ancestry; Yoruba people in Nigeria; and Han Chinese in Beijing.

The variations in the progesterone receptor gene — consisting of single nucleotide polymorphisms, or one-letter changes in the genetic code — were found in regions of the gene that regulate when it is switched on and off.

Recent natural selection took the genetic code in different directions as different populations adapted to their local environments, the scientists found. The sequence in Han Chinese populations had an evolutionarily new variation, perhaps reflecting that premature birth would have been especially costly for the small group of ancestral humans who migrated from Africa to East Asia. In contrast, modern populations with European and African ancestry had a greater mixture reflecting new and ancestral versions in the gene. 

The findings also predict that the genetic forms of the progesterone receptor seen in East Asians would not necessarily protect against premature birth in other populations. The researchers confirmed this prediction with data from 1,733 African-American women enrolled in a study called the Boston Birth Cohort; of these women, 461 had spontaneous preterm births and 237 had medically indicated preterm births, in which doctors deliver the baby early because of medical problems that have developed during pregnancy for the mother, fetus or both. African-American women who had genetic variants typically seen in East Asian populations had a higher risk of premature birth, the study found.

Genes alone don’t determine risk

The study’s underlying message is that genes that are helpful in one environment may not help in another, Shaw said. “Complex conditions such as prematurity are not likely caused completely environmentally or completely genetically; it’s the confluence of genes and environment that makes the difference in risk,” he said.

The researchers also examined the progesterone receptor in genetic data from four female Neanderthals — one that lived about 122,000 years ago, and three that lived about 52,000 years ago. These individuals had a version of the receptor linked to a high risk of preterm birth. This version of the gene may have been introduced to early human populations by interbreeding between humans and Neanderthals, the findings suggest.

This type of information may help us develop personalized approaches to preventing preterm birth.

Next, the researchers plan to study pregnant women who have received progesterone to try to prevent premature birth. “We want to determine whether genetic differences in the receptor could explain why giving the hormone prevents premature delivery in some women but not others,” Stevenson said. “This type of information may help us develop personalized approaches to preventing preterm birth.”

Michael Snyder, PhD, professor of genetics, is also a Stanford author of the paper. Shaw, Stevenson and Snyder are members of the Stanford Child Health Research Institute and of Stanford Bio-X. Stevenson is an affiliate of the Stanford Woods Institute for the Environment, and Snyder is a member of the Stanford’s Cardiovascular Institute, its Cancer Institute and its Neurosciences Institute.

Scientists at Johns Hopkins University, Case Western Reserve University and the University of Cincinnati also contributed to the study.

The study was funded by March of Dimes Prematurity Research Center at Stanford University School of Medicine, the National Heart, Lung and Blood Institute (grant RC2 HL101748), the National Institutes of Health (grant 5P50HG00773502) and the California Institute for Regenerative Medicine (grant GC1R-06673-A).

Stanford’s Department of Pediatrics also supported the work.

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