Abstract
Uncomplicated healthy pregnancy is the outcome of successful fertilization, implantation of embryos, trophoblast development and adequate placentation. Any deviation in these cascades of events may lead to complicated pregnancies such as preeclampsia (PE). The current incidence of PE is 2–8% in all pregnancies worldwide, leading to high maternal as well as perinatal mortality and morbidity rates. A number of randomized controlled clinical trials observed the association between low dose aspirin (LDA) treatment in early gestational age and significant reduction of early onset of PE in high-risk pregnant women. However, a substantial knowledge gap exists in identifying the particular mechanism of action of aspirin on placental function. It is already established that the placental-derived exosomes (PdE) are present in the maternal circulation from 6 weeks of gestation, and exosomes contain bioactive molecules such as proteins, lipids and RNA that are a “fingerprint” of their originating cells. Interestingly, levels of exosomes are higher in PE compared to normal pregnancies, and changes in the level of PdE during the first trimester may be used to classify women at risk for developing PE. The aim of this review is to discuss the mechanisms of action of LDA on placental and maternal physiological systems including the role of PdE in these phenomena. This review article will contribute to the in-depth understanding of LDA-induced PE prevention.
Highlights
Pregnancy is an important event that leads to significant changes in maternal physiology
Tannetta et al observed that syncytiotrophoblast derived extracellular vesicles (STBEVs) that are placental alkaline phosphatase (PLAP) positive inhibit the aggregation of platelets that were treated with aspirin [218]
Several studies focused on extracellular vesicles (EVs) highlighting their extraordinary characteristics as natural carriers of bioactive molecules, which can be used as biomarker for several pathological conditions including PE
Summary
Pregnancy is an important event that leads to significant changes in maternal physiology. The broad concept of PE pathophysiology includes defective trophoblast invasion and inadequate uterine spiral arterial remodeling in the first trimester that follows with reduced uteroplacental perfusion [3] This subsequently leads to poorly perfused and stressed placental syncytiotrophoblasts that release a range of mediators causing endothelial dysfunction and PE clinical manifestations [3]. Placental syncytiotrophoblast release extracellular vesicles (EVs) including exosomes into the maternal bloodstream that contain some information (i.e., micro RNA, mRNA, proteins) to convey from the originating cells to their distant target cells such as maternal immune cells in order to adapt to the pregnancy associated physiological changes [17] This EV release is further increased from the preeclamptic placenta due to oxidative stress, causing widespread systemic endothelial dysfunction, giving rise to maternal hypertension, feto-placental circulatory compromise and damaging various maternal organs [17]. Maternal serum biochemical markers of pregnancy, namely alpha fetoprotein (AFP), human chorionic gonadotrophin (hCG), unconjugated estriol [24] and inhibin-A [25], are produced and found in higher concentration in the maternal peripheral circulation due to the implantation and placentation processes of pregnancy
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