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‘Guardian angel gene’ key to avoiding premature births
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Removal of an essential gene was a major contributor to preterm labor, according to recent research.
Researchers from Cincinnati Children’s Hospital Medical Center started with a pathway linked to the tumor suppressor gene known as transformation-related protein 53 (Trp53), which encodes another protein: p53. Mutations of Trp53 are found in a variety of cancers, but the gene’s function in female reproduction and other normal physiological processes is not well understood. The role of p53, sometimes referred to as the “guardian angel gene,” is to help preserve genetic stability and prevent mutation.
The researchers targeted certain signaling pathways that function both in pregnancy and during the formation of cancerous tumors. During pregnancy, the pathways are usually tightly regulated. In tumor development, however, they can become dysfunctional.
The researchers looked at mice that had the Trp53 gene conditionally deleted in the uterus. They observed that when the mice mated with fertile males, they had normal ovulation, fertilization and embryo implantation. Deficiency of p53, however, activated other signaling pathways in the uterus (involving the proteins pAkt and p21) that set the stage for premature birth.
“Preterm birth and prematurity 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,” Sudhansu K. Dey, PhD, a study researcher from the center, said in a press release.
Funding support came in part from the National Institutes of Health, and Yasushi Hirota, PhD, receives funding support from the Japanese Society for the Promotion of Science Postdoctoral Fellowships for Research Abroad. Additional information can be found at cincinnatichildrens.org.
Dey S. J Clin Invest. 2010;doi:10.1172/JCI40051.