A protein deficiency triggered by a gene plays a role in premature births

By Peggy O’Farrel
Source: Cincinnati News

A protein deficiency triggered by a gene that’s supposed to prevent the growth of cancerous tumours plays a role in premature births; say Cincinnati Children’s Hospital Medical Centre researchers.

An intubated female premature infant born prem...

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The discovery is one of the first that gives experts a target on which to focus future research into why babies are born early, and it could ultimately guide efforts to prevent that, said Sudhansu K. Dey, director of reproductive sciences at Cincinnati Children’s and the study’s senior investigator.

“Pre-term birth and prematurely are problems that pose huge long-term social and economic liabilities, and there is an urgent need for research with new approaches to combat this public health concern,” he said.

Premature birth accounts for about 30 percent of all newborn deaths, and costs about $26 billion a year in the U.S., according to the Institute of Medicine.

In Hamilton County, about 16 percent of babies are born prematurely, compared to about 13 percent nationally.

For the study, Dey and his team targeted the molecular interactions that allow cells to communicate. The interactions are tightly regulated during pregnancy, but become dysfunctional when tumours develop.

Dey and his team looked at the interactions linked to a tumour-suppressor gene, which controls the actions of a second gene, called p53. Sometimes called “the guardian angel gene,” p53 protects genetic stability and prevents genetic mutations.

Scientists already know that mutations of the suppressor-suppressor gene are found in some cancers, but little is known about its role in pregnancy and other body processes.

To understand the role p53 plays in female reproduction, Dey and his team designed genetically altered mice missing the suppressor-suppressor gene. The missing gene meant the mice couldn’t produce p53.

When the genetically altered mice mated with normal male mice, most stages of conception and pregnancy were normal.

But the p53 deficiency set off a series of processes that led to premature birth, including causing cells designed to support the foetus and grow protective placenta to form improperly.

Those improperly formed cells, in turn, triggered the release of the enzyme COX2 and that caused the mice’s uterine muscles to contract, leading to pre-term birth.

More than half of the genetically altered mice experienced pre-term birth and the death of their newborn offspring.

The findings were striking because doctors often give women celecoxib, a drug that counteracts COX2, to prevent premature birth.

Doctors know a lot about the socio-economic factors – lack of prenatal care, substance abuse, use of fertility treatments that lead to multiple births – that contribute to premature birth, said Jeffrey Whitsett, a researcher at Cincinnati Children’s.

But they know very little about the biological processes that trigger childbirth, whether it’s premature or right on time, he said.

“We don’t even know whether the mother signals the baby to be born or the baby signals the mother,” he said.

Discovery of the role p53 plays in triggering premature birth in mice “really gives us, for the first time, a handhold in knowing where to look.”

Kim Brady, director of obstetrics at Good Samaritan Hospital, said he’d be interesting in seeing the research translated to women. If the findings are applicable in people, he said, women who’ve had premature babies should have p53 deficiencies.

The findings could explain why some groups are more prone to premature birth, he said, and could help doctors determine who’s likely to need treatment to prevent premature births.

“It really opens up the opportunity for future research,” he said.

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