CD74-Downregulation of Placental Macrophage-Trophoblastic Interactions in Preeclampsia

Przybył, L; Haase, Nadine; Golić, Michaela; Rugor, Julianna; Solano, María Emilia; Arck, Petra C.; Gauster, Martin; Huppertz, Berthold; Emontzpohl, Christoph; Stoppe, Christian; Bernhagen, Jürgen; Leng, Lin; Bucala, Richard; Schulz, Herbert; Heuser, Arnd; Weedon-Fekjær, M.S.; Johnsen, Guro M.; Peetz, D.; Luft, Friedrich C.; Staff, Anne Cathrine; Müller, Dominik N.; Dechend, Ralf; Herse, Florian

doi:10.1161/circresaha.116.308304

Cited by 69 publications

(56 citation statements)

References 59 publications

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“…Severity of preeclampsia pathology is also a leading cause of preterm birth. Thus, if an altered immune system contributes to the systemic and local symptoms of preeclampsia [11][12][13][14][15][16][17][18][19][20][21][22], it is tempting to speculate that the same or diverse underlying immune changes may predispose to different phenotypes of the syndrome. Dysregulation of immunity in preeclampsia is thought to start with inadequate immune tolerance to paternal alloantigens present on trophoblasts.…”

Section: Introductionmentioning

confidence: 99%

“…Nevertheless, recent data suggest that the defective immune intolerance to the conceptus may be involved through primary and secondary immune responses. Although a considerable number of reviews have already focused on different aspects of immune responses including the role of macrophages in preeclampsia [11][12][13][14][15][16][17][18][19][20][21][22], this review will provide contemporary discussion on NK cells and regulatory T cells (Tregs) and their participation in the pathology of this pregnancy complication. A focus on NK cells and Tregs can be rationalized because NK cells predominantly populate the pregnant uterus and guide trophoblast invasion whereas Tregs are recruited to the endometrium in response to hormones to establish immune tolerance.…”

Section: Introductionmentioning

confidence: 99%

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Preeclampsia and health risks later in life: an immunological link

Cheng

Sharma

2016

Semin Immunopathol

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Pregnancy represents a period of physiological stress, and although this stress is experienced for a very modest portion of life, it is now recognized as a window to women's future health, often by unmasking predispositions to conditions that only become symptomatic later in life. In normal pregnancy, the mother experiences mild metabolic syndrome-like condition through week 20 of gestation. A pronounced phenotype of metabolic syndrome may program pregnancy complications such as preeclampsia. Preeclampsia is a serious complication with a myriad of manifestations for mother and offspring. This pregnancy syndrome is a polygenic disease and has been now linked to higher incidence of cardiovascular disease, diabetes, and several other disorders associated with vulnerable organs. Furthermore, the offspring born to preeclamptic mothers also exhibit an elevated risk of cardiovascular disease, stroke, and mental disorders during adulthood. This suggests that preeclampsia not only exposes the mother and the fetus to complications during pregnancy but also programs chronic diseases in later life. The etiology of preeclampsia is thought to be primarily associated with poor placentation and entails excessive maternal inflammation and endothelial dysfunction. It is well established now that the maternal immune system and the placenta are involved in a highly choreographed cross-talk that underlies adequate spiral artery remodeling required for uteroplacental perfusion and free flow of nutrients to the fetus. Since normal pregnancy is associated with a sequence of events represented by temporal events of inflammation (implantation), anti-inflammation (gestation), and inflammation (parturition), it is quite possible that unscheduled alterations in these regulatory responses may lead to pathologic consequences. Although it is not clear whether immunological alterations occur early in pregnancy, it is proposed that dysregulated systemic and placental immunity contribute to impaired angiogenesis and the onset of preeclampsia. This review will focus on important aspects of the immune system that coordinate with placental dysfunction to program preeclampsia and influence health in later life.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Preeclampsia and health risks later in life: an immunological link

Cheng

Sharma

2016

Semin Immunopathol

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“…Real-time quantitative (q)PCR was done as described previously [33]. Total mRNA was isolated using QIAzol lysis reagent and Qiagen RNeasy mini kit (Qiagen) according to the manufacturer's protocol, followed by deoxyribonuclease I (Qiagen) treatment.…”

Section: Methodsmentioning

confidence: 99%

Protective Function of Ahnak1 in Vascular Healing after Wire Injury

Haase

Rüder²,

Haase³

et al. 2017

J Vasc Res

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Aim: Vascular remodeling following injury substantially accounts for restenosis and adverse clinical outcomes. In this study, we investigated the role of the giant scaffold protein Ahnak1 in vascular healing after endothelial denudation of the murine femoral artery. Methods: The spatiotemporal expression pattern of Ahnak1 and Ahnak2 was examined using specific antibodies and real-time quantitative PCR. Following wire-mediated endothelial injury of Ahnak1-deficient mice and wild-type (WT) littermates, the processes of vascular healing were analyzed. Results: Ahnak1 and Ahnak2 showed a mutually exclusive vascular expression pattern, with Ahnak1 being expressed in the endothelium and Ahnak2 in the medial cells in naïve WT arteries. After injury, a marked increase of Ahnak1- and Ahnak2-positive cells at the lesion site became evident. Both proteins showed a strong upregulation in neointimal cells 14 days after injury. Ahnak1-deficient mice showed delayed vascular healing and dramatically impaired re-endothelialization that resulted in prolonged adverse vascular remodeling, when compared to the WT littermates. Conclusion: The large scaffold and adaptor proteins Ahnak1 and Ahnak2 exhibit differential expression patterns and functions in naïve and injured arteries. Ahnak1 plays a nonredundant protective role in vascular healing.

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“…The transcriptomic and protein expression of CD74, a HLA class II molecule, are decreased in placental macrophages of preeclampsia women. This down-regulation of CD74 interferes with trophoblast-macrophage cross-talk [138]. Prins et al investigated macrophages in early decidua from women who later developed preeclampsia [139].…”

Section: Preeclampsiamentioning

confidence: 99%

Gene Expression Profiling of Placenta from Normal to Pathological Pregnancies

Mezouar¹,

Mège²

2018

Placenta

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The placenta is a unique temporary organ essential for growth of the fetus, which determines the success of pregnancy. Its originality relies on a combination of nutritive, endocrine and immunological functions that control maternal immune tolerance to fetus. In the present chapter, we review gene expression programs of placenta from placenta tissue to isolated cells using high throughput transcriptomic approach. Beside trophoblasts, we focused on immune cells including macrophages, dendritic cells and mast cells. From the gene expression signatures, we identify key pathways for the different trimesters of the normal pregnancy and pathological alterations including preeclampsia and gestational diabetes mellitus.

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CD74-Downregulation of Placental Macrophage-Trophoblastic Interactions in Preeclampsia

Cited by 69 publications

References 59 publications

Preeclampsia and health risks later in life: an immunological link

Preeclampsia and health risks later in life: an immunological link

Protective Function of Ahnak1 in Vascular Healing after Wire Injury

Gene Expression Profiling of Placenta from Normal to Pathological Pregnancies

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