NIH Record - National Institutes of Health

Atlas of Placenta May Yield New Clues

A mother holds an infant

Photo:  PHOTO: KIEFERPIX/SHUTTERSTOCK

An atlas revealing the activity of individual placental cells during childbirth offers insight on what happens at the maternal-fetal interface during term labor, according to an NIH-supported study. The work, led by researchers at NICHD, is published in Science Translational Medicine.

The atlas provides a single-cell analysis of the human placenta and its surrounding membranes and is the first to use this method to understand the communication that occurs between maternal and fetal cells during the process of labor. Studying these processes aids understanding of typical labor and delivery at term, as well as preterm labor and delivery, which occurs before 37 weeks of pregnancy and is a leading cause of infant death and long-term disability. 

The study team created the placental atlas by using single-cell RNA sequencing, which examines the activity and signaling patterns of individual cells. The atlas, based on samples from 42 term pregnancies, describes changes in gene expression patterns among the different cell types in the placenta and its surrounding membranes including both maternal and fetal-derived cells.

Researchers found that cells most affected by labor were in the chorioamniotic membranes, which surround the fetus and rupture as part of the labor and delivery process. 

Scientists also found that fetal stromal and maternal decidual cells were particularly active in generating inflammatory signaling. These findings are consistent with previous research showing that inflammation (unrelated to infection) is important for sustaining labor.

The study is also a proof-of-concept that placental biomarkers present in maternal blood may be used to identify pregnancies at risk for preterm birth. Researchers used the atlas to classify cell-specific signatures of labor, which were detectable in maternal blood samples from term and preterm pregnancies. 

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Staff Writer: Amber Snyder
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