Role of Tissue Factor in the Maternal Immunological Attack of the Embryo in the Antiphospholipid Syndrome

Girardi, Guillermina

doi:10.1007/s12016-009-8187-1

Cited by 31 publications

(21 citation statements)

References 50 publications

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“…During trophoblast differentiation, aPL activates complement via the classical pathway. Complement activation (C3 and C5a) directly mediates placental injury and causes fetal loss and growth restriction, resulting from an imbalance of angiogenic factors (e.g., VEGF and placental growth factor) as well as their corresponding receptors that are required for normal placental development [234]. …”

Section: Coagulation-dependent Events: Thrombosis/inflammation-assmentioning

confidence: 99%

Tissue Factor, Blood Coagulation, and Beyond: An Overview

Chu

2011

International Journal of Inflammation

180

184

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Emerging evidence shows a broad spectrum of biological functions of tissue factor (TF). TF classical role in initiating the extrinsic blood coagulation and its direct thrombotic action in close relation to cardiovascular risks have long been established. TF overexpression/hypercoagulability often observed in many clinical conditions certainly expands its role in proinflammation, diabetes, obesity, cardiovascular diseases, angiogenesis, tumor metastasis, wound repairs, embryonic development, cell adhesion/migration, innate immunity, infection, pregnancy loss, and many others. This paper broadly covers seminal observations to discuss TF pathogenic roles in relation to diverse disease development or manifestation. Biochemically, extracellular TF signaling interfaced through protease-activated receptors (PARs) elicits cellular activation and inflammatory responses. TF diverse biological roles are associated with either coagulation-dependent or noncoagulation-mediated actions. Apparently, TF hypercoagulability refuels a coagulation-inflammation-thrombosis circuit in “autocrine” or “paracrine” fashions, which triggers a wide spectrum of pathophysiology. Accordingly, TF suppression, anticoagulation, PAR blockade, or general anti-inflammation offers an array of therapeutical benefits for easing diverse pathological conditions.

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Section: Coagulation-dependent Events: Thrombosis/inflammation-assmentioning

confidence: 99%

Tissue Factor, Blood Coagulation, and Beyond: An Overview

Chu

2011

International Journal of Inflammation

180

184

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“…Transient but significant increase of blood TNFa levels was also reported. 6 On the other hand, inhibition of complement cascade in vivo, using the C3 convertase inhibitor complement receptor 1-related gene/protein y (Crry)-Ig, protects animals from the aPL-mediated effects. Complement C3 defect displays a comparable protective effect.…”

Section: Thrombotic Mechanismsmentioning

confidence: 99%

Anti-phospholipid antibody mediated fetal loss: still an open question from a pathogenic point of view

Meroni

Tedesco

Locati

et al. 2010

Lupus

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Antiphospholipid antibodies (aPL) are associated with recurrent miscarriages and pregnancy complications, however their pathogenic mechanisms are still matter of research. Thrombotic events at the placental level cannot explain all of the clinical manifestations. It has been suggested that aPL may be responsible for a local acute inflammatory response mediated by complement activation and neutrophil infiltration eventually leading to fetal loss. However histological and immunohistological studies on human placental samples do support such a mechanism only in part and with no any clear relationship with the pregnancy outcome. A direct effect of aPL on both maternal and fetal placental tissues has been reported through the reactivity of the antibodies with beta2 glycoprotein I (beta2GPI) expressed on the cell membranes. These events do not require an inflammatory response and can be in part related to the inhibition of growth factors favouring a physiological placentation. Understanding the different pathogenic mechanisms of aPL-associated miscarriages may help in improving our therapeutic approach particularly in recurrent cases not responsive to the usual treatment.

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“…It has been suggested that cellular functions of the trophoblast would be altered, thus leading to defective placentation and playing a crucial pathogenic role in obstetric complications in the APS, by non-thrombotic mechanisms [5,[13][14][15]. At the same time, the formation of immune complexes a-β2GP1 can activate the classical pathway of complement system and induce localized immune damage [16]. It has been demonstrated in vitro that binding of a-β2GP1 to the syncytiotrophoblast affects its invasive capacity [17] and decreases human chorionic gonadotrophin synthesis [18,19].…”

Section: Introductionmentioning

confidence: 99%

Antiphospholipid and antioangiogenic activity in females with recurrent miscarriage and antiphospholipid syndrome

et al. 2016

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Ethical approval: The study was approved by the Bioethics Comitee of Facultad de Ciencias Bioquímicas y Farmacéuticas (Universidad Nacional de Rosario). Res Nº 076/2008. All participants signed the corresponding informed consent. Guarantor: SMMA Contributorship: HFP performed most assays and analysis of results, and wrote the paper. EP and CB performed some assays and collaborated in the analysis of results. JM performed patients selection for the study and aided in medical matters. MB, MJS and SMD performed sample collection and conditioning, as well as some laboratory determinations. HB performed statistical analysis. SMMA coordinated and supervised the whole study. Abstract word count: 251. Actual word count (excluding abstract and references): 2664 AbstractBackground: Antiphospholipid syndrome (APS) is an autoimmune disease characterized by thrombosis, fetal losses and thrombocytopenia associated to antiphospholipid (APL) antibodies (Abs). They are directed to phospholipids, such as cardiolipins (a-cardiolipin, ACA) and lupus anticoagulant (LA), or to complexes formed by phospholipids and protein cofactors, such as β2 glycoprotein 1 (a-β2GP1) and annexin V (a-annexin V). These auto Abs may be considered as a family of Abs involved in thrombotic events and APL activity. On the other hand, some proangiogenic factors are involved in the normal development of placental vasculature, such as the vascular endothelial growth factor (VEGF). Overexpression of VEGF receptor in its soluble form (sVEGFR-1) has been associated to a higher antiangiogenic activity. Our aim was to analyze the association between ACA, LA, a-β2GP1, a-annexin V and sVEGFR-1 with recurrent miscarriage before week 10 of gestation in women with APS. Methods: We studied 24 women (primary or secondary APS), who were divided into two groups: women with recurrent miscarriage before week 10 of gestation [M; n=12] and women with no history of fetal loss [NM; n=12]. ACA, a-β2GP1, aannexin V and sVEGF-R1 levels were assessed by ELISA, while LA was assessed by screening and confirmatory tests. Results: A significant association was observed between the number of positive biomarkers and the belonging group (p<0.05). Besides, a positive result for LA and a-β2GP1 was found to be significantly associated to the M group (p<0.05). Conclusions: LA and a-β2GP1 may be implicated in pregnancies complicated by recurrent miscarriage in women with APS.

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Role of Tissue Factor in the Maternal Immunological Attack of the Embryo in the Antiphospholipid Syndrome

Cited by 31 publications

References 50 publications

Tissue Factor, Blood Coagulation, and Beyond: An Overview

Tissue Factor, Blood Coagulation, and Beyond: An Overview

Anti-phospholipid antibody mediated fetal loss: still an open question from a pathogenic point of view

Antiphospholipid and antioangiogenic activity in females with recurrent miscarriage and antiphospholipid syndrome

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