Particle Clusters Named a Culprit in Premature Birth (2 of 2) (IMAGE)
Caption
This schematic illustration shows the proposed process of calciprotein particle (CPP) formation in amniotic fluid (AF) and resultant pathogenic effects on fetal membranes. (1) Assembly: fetuin-A binds hydroxyapatite (HA) in AF, forming colloidal intermediate CPPs. (2) Aggregation: soluble CPPs aggregate into insoluble mature CPPs that trap and deplete other AF proteins. (3) Deposition: mature CPPs precipitate out of solution and deposit in fetal membranes. (4) Pathogenic effects: pathogenic effects of CPPs include amnion epithelial apoptosis, ectopic osteogenesis of amnion fibroblasts, local prostaglandin release, and extracellular matrix degradation resulting in a loss of membrane strength and elasticity. The red-colored cell indicates osteoblastic trans-differentiation. This material relates to a paper that appeared in the Nov. 9, 2016, issue of Science Translational Medicine, published by AAAS. The paper, by L.L. Shook at Yale University School of Medicine in New Haven, CT, and colleagues was titled, "Calciprotein particles as potential etiologic agents of idiopathic preterm birth."
Credit
L.L. Shook <i>et al., Science Translational Medicine</i> (2016)
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