CINCINNATI, Oct. 24, 2011 /PRNewswire-USNewswire/ -- Scientists who developed a novel mouse model mimicking human preterm labor have described a molecular signaling pathway underlying preterm birth and targeted it to stop the problem.
In a study to be published online the week of Oct. 24 by PNAS (Proceedings of the National Academy of Sciences), the researchers report their findings may lead to new strategies for combating this major global health issue in humans. The study was led by scientists in the division of Reproductive Sciences and Perinatal Institute at Cincinnati Children's Hospital Medical Center.
They point to molecular signals from the protein complex mTORC1 (mammalian target of rapamycin complex 1). In laboratory tests, the signals contributed to early aging in uterine cells, preterm labor and stillbirth in the genetically modified mice. When researchers gave the mice a low dose of rapamycin – a known inhibitor of mTORC1 signaling – it stopped the early aging of uterine cells and premature birth.
"Our findings show an unanticipated role for mTORC1 signaling in preterm birth in mice and may help us better understand the mechanism of birth timing in humans," says Sudhansu K. Dey, PhD., who led the study and is director of Reproductive Sciences at Cincinnati Children's. "Whether these findings have direct relevance in human birth requires further investigation, although these data could help us develop new and improved strategies to combat this international health problem."
Among a wide array of adverse effects, premature birth can result in underdeveloped organs and organ systems – especially in the respiratory system. It also creates a greater risk for cerebral palsy, as well as learning and developmental disabilities. Globally there are nearly 13
|SOURCE Cincinnati Children's Hospital Medical Center|
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