Scientists who developed a mouse model mimicking human preterm labor have described a molecular signaling pathway underlying preterm birth and targeted it to stop the problem, according to a study to be published online by the Proceedings of the National Academy of Sciences.
U.S. researchers point to molecular signals from the protein complex mTORC1. 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., lead author. "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."
The researchers say future studies will probe even deeper into the molecular interactions of mTORC1 in mouse prematurity to see if there may be different molecular targets and opportunities for therapeutic intervention.
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