Expression of placental glycans and its role in regulating peripheral blood NK cells during preeclampsia: a perspective

Abstract

Preeclampsia is a pregnancy-related multisystem disorder characterized by altered trophoblast invasion, oxidative stress, exacerbation of systemic inflammatory response, and endothelial damage. The pathogenesis includes hypertension and mild-to-severe microangiopathy in the kidney, liver, placenta, and brain. The main mechanisms involved in its pathogenesis have been proposed to limit trophoblast invasion and increase the release of extracellular vesicles from the syncytiotrophoblast into the maternal circulation, exacerbating the systemic inflammatory response. The placenta expresses glycans as part of its development and maternal immune tolerance during gestation. The expression profile of glycans at the maternal–fetal interface may play a fundamental role in physiological pregnancy changes and disorders such as preeclampsia. It is unclear whether glycans and their lectin-like receptors are involved in the mechanisms of maternal–fetal recognition by immune cells during pregnancy homeostasis. The expression profile of glycans appears to be altered in hypertensive disorders of pregnancy, which could lead to alterations in the placental microenvironment and vascular endothelium in pregnancy conditions such as preeclampsia. Glycans with immunomodulatory properties at the maternal–fetal interface are altered in early-onset severe preeclampsia, implying that innate immune system components, such as NK cells, exacerbate the systemic inflammatory response observed in preeclampsia. In this article, we discuss the evidence for the role of glycans in gestational physiology and the perspective of glycobiology on the pathophysiology of hypertensive disorders in gestation.

Microplastics from disposable paper cups are enriched in the placenta and fetus, leading to metabolic and reproductive toxicity during pregnancy

“…5d, e and Supplementary Fig. 11b), why may implicate reproductive complications, including preeclampsia, intrauterine growth restriction, and an increased risk of miscarriage (49)(50)(51). Conversely, we observed a downregulation of pathways involved in lipid metabolism, phosphatidylinositol signaling, inositol phosphate metabolism, and ABC transporters (Fig.…”

Features and Comparative Characteristics of Fucosylated Glycans Expression in Endothelial Glycocalyx of Placental Terminal Villi in Patients with Preeclampsia Treated with Different Antihypertensive Regimens

“…Hypoxia may be one of these factors, since it (i) results from placental pathology, which is caused by morphologic or occlusivestenotic malformations of the vessels of fetoplacental complex, and is a characteristic sign of early-onset and late-onset PE; (ii) is both a factor that stimulates the development of sterile systemic inflammation and endothelial dysfunction in response to placental damage [35,36], and a factor destabilizing the eGC [37][38][39], thus leading to hemodynamic disorders; (iii) is one of the key stimulating factors of angiogenesis [40,41], which is impaired in patients with placenta-associated complications of pregnancy, in particular, PE and FGR [42,43]; and (iv) is a regulator of glycan expression in human placental structures [44] (in particular, hypoxia stimulates the expression of fucosylated glycans on the surface of endothelial cells) [45,46]. It should also be noted that, in addition to hypoxia, changes in the expression of glycans, including fucoglycans, activate pro-inflammatory factors [47,48]. Based on the above facts, we suggested that the expression of fucosylated glycans in the eGC of fetal capillaries of the placental terminal villi is connected with maternal and fetoplacental hemodynamic parameters, as well as with the factors reflecting the degree of development of systemic inflammatory response and endothelial dysfunction.…”