Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease

Wang, X

doi:10.1016/s1470-0328(02)01929-8

Cited by 5 publications

(6 citation statements)

References 21 publications

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“…T-cell anergy to fetal antigens has been associated with the IL-10 regulatory and tolerant properties of decidual macrophages ( 29 ). IL-10 therapy of T. gondii infections reduces trophoblasts apoptosis at the maternal–fetal interface and improves pregnancy outcomes ( 38 , 39 ). Decidual macrophage LILRB4 ligation by FcγRI inhibited TNF-α production and hampered functional activation ( 17 ).…”

Section: Discussionmentioning

confidence: 99%

Decidual Macrophage Functional Polarization during Abnormal Pregnancy due to Toxoplasma gondii: Role for LILRB4

Zhao

et al. 2017

Front. Immunol.

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During gestation, Toxoplasma gondii infection produces a series of complications including stillbirths, abortions, and congenital malformations. The inhibitory receptor, LILRB4, which is mainly expressed by professional antigen-presenting cells (especially macrophages and dendritic cells) may play an important immune-regulatory role at the maternal–fetal interface. To assess the role of LILRB4 during T. gondii infection, LILRB4−/− and T. gondii infected pregnant mouse models were established. Further, human primary-decidual macrophages were treated with anti-LILRB4 neutralizing antibody and then infected with T. gondii. These in vivo and in vitro models were used to explore the role of LILRB4 in T. gondii-mediated abnormal pregnancy outcomes. The results showed that abnormal pregnancy outcomes were more prevalent in LILRB4−/− infected pregnant mice than in wild-type infected pregnant mice. In subsequent experiments, expression levels of LILRB4, M1, and M2 membrane-functional molecules, arginine metabolic enzymes, and related cytokines were assessed in uninfected, infected, LILRB4-neutralized infected, and LILRB4−/− infected models. The results demonstrated T. gondii infection to downregulate LILRB4 on decidual macrophages, which strengthened M1 activation functions and weakened M2 tolerance functions by changing M1 and M2 membrane molecule expression, synthesis of arginine metabolic enzymes, and cytokine secretion profiles. These changes contributed to abnormal pregnancy outcomes. The results of this study provide not only a deeper understanding of the immune mechanisms operational during abnormal pregnancy, induced by T. gondii infection, but also identify potential avenues for therapeutic and preventive treatment of congenital toxoplasmosis.

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Section: Discussionmentioning

confidence: 99%

Decidual Macrophage Functional Polarization during Abnormal Pregnancy due to Toxoplasma gondii: Role for LILRB4

Zhao

et al. 2017

Front. Immunol.

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“…Endothelial cells in different beds do vary in the capacity to express adhesion proteins. We have previously shown that the expression of nitric oxide synthase mRNA is increased in endothelial cells induced by factor(s) released into the fetal circulation in umbilical placental vascular disease 7 . Nitric oxide has been reported to inhibit the induction of VCAM-1 expression by endothelial cells stimulated by factors such as cytokines 10 .…”

Section: Discussionmentioning

confidence: 99%

“…Platelet activation and consumption also occurs in this group. We have shown that plasma from fetuses with Doppler evidence of umbilical placental vascular disease contains factor(s) that induces endothelial cell apoptosis and up-regulates mRNA expression of nitric oxide synthase 6,7 .…”

Section: Introductionmentioning

confidence: 99%

Endothelial cell expression of adhesion molecules is induced by fetal plasma from pregnancies with umbilical placental vascular disease

Wang¹

2002

BJOG: An International Journal of Obstetrics and Gynaecology

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Objective To test the hypothesis that local production with spill into the fetal circulation of factor(s) injurious to endothelium is responsible for the vascular pathology present when the umbilical artery Doppler study is abnormal. Expression of adhesion molecules is a feature of endothelial cell activation. Design Case -control study.Setting University teaching hospital.Samples Fetal plasma was collected from 27 normal pregnancies, 39 pregnancies with umbilical placental vascular disease defined by abnormal umbilical artery Doppler and 11 pregnancies with pre-eclampsia and normal umbilical artery Doppler. Methods Isolated and cultured human umbilical vein endothelial cells from normal pregnancies were incubated with fetal plasma from three study groups. mRNA expression of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and platelet-endothelial cell adhesion molecule-1 (PECAM-1) were assessed by reverse transcription-polymerase chain reaction. To confirm the occurrence of this in vivo, we measured the levels of soluble fractions of sICAM-1, sVCAM-1 and sPECAM-1 in the fetal circulation in the fetal plasma used for endothelial cell incubation. Results The mRNA expression of ICAM-1 [median 1.1 (interquartile range 0.5-1.9) vs 0.7 (0.3 -1.2), P < 0.05] and PECAM-1 [2.1 (1.2 -3.0) vs 1.5 (0.7 -2.1), P < 0.05] was significantly higher following incubation with fetal plasma from umbilical placental vascular disease compared with the normal group. There was no difference in the expression of VCAM-1 [1.2 (0.9 -1.8) vs 1.1 (0.8 -1.6), ns]. The group with maternal preeclampsia and normal umbilical artery Doppler did not differ from the normal group. In the umbilical placental vascular disease group, the results were similar in the presence or absence of pre-eclampsia. For soluble fractions of the adhesion molecules released into the fetal circulation, we found the levels (ng/mL) of sICAM-1 [median 248.5 (interquartile range 197.3 -315.7) vs 174.2 (144.5 -212.9), P < 0.05] and sPECAM-1 [9.3 (6.2 -11

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“…Giannubilo and colleagues [30] found that eNOS protein levels negatively correlate with the pulsatility Index (PI) determined by Doppler ultrasound, whilst iNOS levels in IUGR placental endothelium show a positive correlation with PI. Additionally, normal HUVEC exposed to PE-derived umbilical plasma show higher iNOS expression [176]. Under these conditions increased levels of nitrosative stress have been described [99].…”

Section: Placental Vascular Reactivity and Nitric Oxide Synthesis In mentioning

confidence: 96%

Role of nitric oxide in placental vascular development and function

Krause¹,

Hanson²,

Casanello³

2011

Placenta

182

122

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Nitric oxide (NO) is one of the most pleiotropic signaling molecules at systemic and cellular levels, participating in vascular tone regulation, cellular respiration, proliferation, apoptosis and gene expression. Indeed NO actively participates in trophoblast invasion, placental development and represents the main vasodilator in this tissue. Despite the large number of studies addressing the role of NO in the placenta, its participation in placental vascular development and the effect of altered levels of NO on placental function remains to be clarified. This review draws a time-line of the participation of NO throughout placental vascular development, from the differentiation of vascular precursors to the consolidation of vascular function are considered. The influence of NO on cell types involved in the origin of the placental vasculature and the expression and function of the nitric oxide synthases (NOS) throughout pregnancy are described. The developmental processes involved in the placental vascular bed are considered, such as the participation of NO in placental vasculogenesis and angiogenesis through VEGF and Angiopoietin signaling molecules. The role of NO in vascular function once the placental vascular tree has developed, in normal pregnancy as well as in pregnancy-related diseases, is then discussed.

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Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease

Cited by 5 publications

References 21 publications

Decidual Macrophage Functional Polarization during Abnormal Pregnancy due to Toxoplasma gondii: Role for LILRB4

Decidual Macrophage Functional Polarization during Abnormal Pregnancy due to Toxoplasma gondii: Role for LILRB4

Endothelial cell expression of adhesion molecules is induced by fetal plasma from pregnancies with umbilical placental vascular disease

Role of nitric oxide in placental vascular development and function

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