Abstract
Two small leucine-rich proteoglycans (SLRP), decorin and biglycan, play important roles in structural–functional integrity of the placenta and fetal membranes, and their alterations can result in several pregnancy-associated diseases. In this review, we briefly discuss normal placental structure and functions, define and classify SLRPs, and then focus on two SLRPs, decorin (DCN) and biglycan (BGN). We discuss the consequences of deletions/mutations of DCN and BGN. We then summarize DCN and BGN expression in the pregnant uterus, myometrium, decidua, placenta, and fetal membranes. Actions of these SLRPs as ligands are then discussed in the context of multiple binding partners in the extracellular matrix and cell surface (receptors), as well as their alterations in pathological pregnancies, such as preeclampsia, fetal growth restriction, and preterm premature rupture of membranes. Lastly, we raise some unanswered questions as food for thought.
Highlights
A Brief Review of the Placental Structure and FunctionsPlacentas in eutherian mammals have evolved to nourish the embryo and the fetus
Since we previously showed that deciduaderived transforming growth factor (TGF)-β provides a key control mechanism limiting trophoblast invasion [41], we suggested that DCN in the decidual ECM serves as a storage device for TGF-β in an inactive form, until cleaved and activated by the trophoblast-derived protease cascade at the invasion front, to prevent over-invasion
We further discovered that selective DCN overproduction by decidual cells, but not villus mesenchymal cells, was associated with PE with or without fetal growth restriction (FGR), and an elevated level of maternal plasma DCN during the second trimester was a predictive biomarker of PE [47]
Summary
Placentas in eutherian mammals have evolved to nourish the embryo and the fetus. For this function, they must invade the pregnant uterus to various degrees. They must invade the pregnant uterus to various degrees They can be broadly classified by their degree of invasiveness into the uterine endometrium: (i) “epitheliochorial” type (in ruminants), in which chorionic trophoblast cells remain apposed to the uterine epithelium, without breaching it. There is evidence of a certain degree of fusion between the trophoblast and the uterine epithelium. In some regions such as chorionic girdles, trophoblast cells are highly invasive (e.g., in horses); (ii) “endotheliochorial” type (in carnivores), in which the trophoblast invades the uterine connective tissue to reach the maternal endothelium; (iii) “hemochorial” type (in rodents, primates, and humans) in which trophoblast cells invade the maternal arteries to derive oxygen and nutrients from the maternal arterial blood. Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations
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