Objective. To examine the expression of hypoxia-inducible factor-1α(HIF-1α), TfR1, and TfR1-attached terminal monosaccharides in placentas of women with IDAP and severe preeclampsia.Methods. TfR1 and HIF-1αwere detected by western blot. Immunoadsorption of TfR1 was performed to characterize the terminal monosaccharides by specific lectin binding.Results. There was no difference in the expression of TfR1 and HIF-1αbetween groups. Lectin blot analysis pointed out an overexpression of galactoseβ1-4N-acetylglucosamine (Gal-GlcNAc) and mannose in severe preeclampsia.Conclusion. The increase in Gal-GlcNAc may be due to the increased presence of antennary structures and the mannose glycans of TfR1 may indicate the presence of misfolded or incomplete proteins. These findings may be associated with the low expression of placental TfR1 in women with preeclampsia.
INTRODUCCIÓN El estado nutricional materno antes y durante la gestación tiene un gran impacto en los resultados materno-fetales (1). El hierro es un nutriente esencial, cofactor de diferentes enzimas del metabolismo (2), necesario para la síntesis de neurotransmisores y la mielinización del sistema nervioso (3) y un componente básico de la hemoglobina y la mioglobina (2). Las alteraciones en el estado de hierro materno durante la gestación se han asociado a enfermedades desde la anemia ferropénica hasta la preeclampsia. La anemia, diagnosticada por una reducción en la concentración de hemoglobina materna (<11g/dl) y de la ferritina sérica (<15ug/L) (4), disminuye la capacidad de trabajo en la madre, aumenta el riesgo de infecciones y el tiempo de tratamiento (5). En el feto, la anemia se ha asociado con restricción de crecimiento intrauterino (RCIU),
This is a case report of women with pregnancy morbidity (PM), some of them associated with antiphospholipid syndrome (APS), in which the glycan patterns of immunoglobulin G (IgG) were investigated based on the theory of alteration of glycosylation in autoimmunity. We used lectin blot to determine changes in terminal glycosylation of polyclonal IgG from women with antiphospholipid (aPL) antibodies and PM plus vascular thrombosis (PM/VT) and seronegative-obstetric APS (SN-OAPS). In addition, we analyzed IgG from women with PM without aPL (PM/aPL-) and healthy women, as controls. Even though the SN-OAPS and PM/VT groups share the PM, only the SN-OAPS group showed a decreased expression of galactose compared to the healthy group. We also found the presence of mannosylated oligosaccharides in IgG from all patients being significantly higher in IgG from women of the PM/aPL - group. The differences in glycans presented here could relate to pathological mechanisms of PM associated with APS.
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.
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