A new study of more than 100 pregnant women pinpoints the abnormal buildup of mineral-protein clusters in amniotic fluid (AF) as a potential culprit in premature birth. The findings open the door to developing therapies or dietary supplements that block the formation of these particles to prevent preterm birth, a leading cause of infant death and disability. Preterm birth is often preceded by premature rupture of fetal membranes, but without an identifiable cause (such as infection or inflammation). In many pregnant women, calcified plaques can be detected in the term or preterm placenta, but their role in premature birth remains elusive. Lydia Shook and colleagues zeroed in on calciprotein particles (CPPs), mineral-protein complexes that have been previously linked to other health complications, including arthritis, atherosclerosis, and aneurism. The researchers analyzed the AF and fetal membranes from study participants who experienced spontaneous preterm birth. They detected greater levels of calcified deposits and reduced levels of a protein that inhibits calcification in individuals with premature membrane rupture compared to a control group that underwent term cesarean sections. Shook et al. discovered the AF from the preterm birth cohort formed CPP aggregates in culture and depleted a number of essential AF proteins. Furthermore, exposure to soluble CPP in vitro impaired the structure and function of fetal membrane samples from women who carried to term, pointing to the particles' toxicity. Future investigations will need to identify triggers that prematurely initiate CPP formation, the authors say.
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Journal
Science Translational Medicine