Glycan expression in chorionic villi from histocultures of women with early-onset preeclampsia: Immunomodulatory effects on peripheral natural killer cells

Campuzano, Marisol; Bueno-Sánchez, Julio César; Agudelo-Jaramillo, Bernardo; Quintana-Castillo, Juan Carlos; Chaouat, G.; Maldonado-Estrada, Juan G

doi:10.1016/j.jri.2020.103212

Cited by 5 publications

(3 citation statements)

References 52 publications

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“…Peripheral mononuclear leukocytes-containing NK cells co-cultured with fresh villous tissue or BeW0 cells showed that CD56Bright NK cells did significantly produce higher concentrations of IFN - γ and TGF-β than CD56Dim NK cells, consistent with a previous report in which circulating CD56dim and CD56bright NK cells exhibited predominantly cytotoxic and cytokine-producing phenotypes, respectively ( 211 ). Besides, blocking glycosylation in a BeWo cell syncytialization model using N -glycosylation inhibitors (e.g., castanomycin and tunicamycin) revealed differences in intracellular IFN-γ production by CD56Bright NK cells in co-culture ( 211 ). It demonstrated that co-culture of primary placental villous tissue with the choriocarcinoma cell line BeWo modulates NK cell function through specific glycan expression.…”

Section: Introductionsupporting

confidence: 90%

“…( 211 ) investigated the effects of placental glycans on NK cell activity using a peripheral NK cell with a full-term human villous tissue co-culture system to assess whether changes in glycosylation profile could account for differences in cytokine production and cytotoxicity. Peripheral mononuclear leukocytes-containing NK cells co-cultured with fresh villous tissue or BeW0 cells showed that CD56Bright NK cells did significantly produce higher concentrations of IFN - γ and TGF-β than CD56Dim NK cells, consistent with a previous report in which circulating CD56dim and CD56bright NK cells exhibited predominantly cytotoxic and cytokine-producing phenotypes, respectively ( 211 ). Besides, blocking glycosylation in a BeWo cell syncytialization model using N -glycosylation inhibitors (e.g., castanomycin and tunicamycin) revealed differences in intracellular IFN-γ production by CD56Bright NK cells in co-culture ( 211 ).…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2023

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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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Section: Introductionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

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

et al. 2023

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“…HLA, Toll-like, or T-cell receptors), and some have multiple N-glycosylation sites [ 64–66 ]. Preconditioning BeWo cells with glycosyltransferase inhibitors (tunicamycin and castanospermine) prior to co-incubation with peripheral blood-derived CD56 bright natural killer (NK) cells can decrease interferon-γ production by the latter, which suggests potential roles for N-glycosylation in modulation of NK cell-mediated inflammatory signaling [ 15 ]. Through actively producing transforming growth factor β1 (immunomodulators with several N-glycosylation sites), primary endovascular EVTs isolated from term placenta can promote differentiation of peripheral CD4 + T cells (from healthy non-pregnant women) into regulatory T cells with immunosuppressive characteristics, while interstitial EVTs and decidual endothelial cells cannot [ 67 ].…”

Section: N-glycosylated Immunomodulators and Galectinsmentioning

confidence: 99%

Roles of N-linked glycosylation and glycan-binding proteins in placentation: trophoblast infiltration, immunomodulation, angiogenesis, and pathophysiology

Huang

Lai

Haslam

et al. 2023

Biochemical Society Transactions

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Protein N-linked glycosylation is a structurally diverse post-translational modification that stores biological information in a larger order of magnitude than other post-translational modifications such as phosphorylation, ubiquitination and acetylation. This gives N-glycosylated proteins a diverse range of properties and allows glyco-codes (glycan-related information) to be deciphered by glycan-binding proteins (GBPs). The intervillous space of the placenta is richly populated with membrane-bound and secreted glycoproteins. Evidence exists to suggest that altering the structural nature of their N-glycans can impact several trophoblast functions, which include those related to interactions with decidual cells. This review summarizes trophoblast-related activities influenced by N-glycan–GBP recognition, exploring how different subtypes of trophoblasts actively adapt to characteristics of the decidualized endometrium through cell-specific expression of N-glycosylated proteins, and how these cells receive decidua-derived signals via N-glycan–GBP interactions. We highlight work on how changes in N-glycosylation relates to the success of trophoblast infiltration, interactions of immunomodulators, and uterine angiogenesis. We also discuss studies that suggest aberrant N-glycosylation of trophoblasts may contribute to the pathogenesis of pregnancy complications (e.g. pre-eclampsia, early spontaneous miscarriages and hydatidiform mole). We propose that a more in-depth understanding of how N-glycosylation shapes trophoblast phenotype during early pregnancy has the potential to improve our approach to predicting, diagnosing and alleviating poor maternal/fetal outcomes associated with placental dysfunction.

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Placenta and maternal endothelium during preeclampsia: Disruption of the glycocalyx explains increased inositol phosphoglycans and angiogenic factors in maternal blood

Scioscia,

Siwetz,

Robillard

et al. 2023

Journal of Reproductive Immunology

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Glycan expression in chorionic villi from histocultures of women with early-onset preeclampsia: Immunomodulatory effects on peripheral natural killer cells

Cited by 5 publications

References 52 publications

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

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

Roles of N-linked glycosylation and glycan-binding proteins in placentation: trophoblast infiltration, immunomodulation, angiogenesis, and pathophysiology

Placenta and maternal endothelium during preeclampsia: Disruption of the glycocalyx explains increased inositol phosphoglycans and angiogenic factors in maternal blood

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