Effects of anti‐endothelial cell antibody in pre‐eclampsia on endothelin‐1 release from cultured endothelial cells

Yamamoto, Tatsuo; Takahashi, Yuko; Kuno, S; Geshi, Yumi; Sasamori, Yukifumi; Mori, Hiroyuki

doi:10.1038/icb.1997.52

Cited by 16 publications

(8 citation statements)

References 21 publications

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“…Expression of TFs on AECA-bound endothelial membrane is associated with thrombosis in several clinical settings, such as preeclampsia, systemic sclerosis, and thrombotic thrombocytopenic purpura [80][81][82]. In KD, AECAs might specifically stimulate endothelial cells in vessels that range in size from the vasa vasorum to medium-sized vessels, resulting in local expression of TF.…”

Section: Autoimmunothrombosis In Kdmentioning

confidence: 99%

Autoimmune Aspects of Kawasaki Disease

Sakurai¹

2019

J Investig Allergol Clin Immunol

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Kawasaki disease (KD) is classified as a medium-sized vasculitis of systemic vasculitis syndrome characterized by hypercytokinemia. Although the etiology of KD remains unidentified, epidemiological features point to the role of infection and genetic predisposition. Recent studies revealed endothelial damage and resultant thrombin generation, as well as B-cell activation during the acute phase of KD. Several anti-endothelial cell autoantibodies (AECAs) have been identified in KD patients. Taken together with the recently developed concept of immunothrombosis, a potential pathogenic mechanism for KD emerges. First, some polyclonal antibodies generated against invading microorganisms would exhibit cross-reactivity toward endothelial cell components and become dominant during affinity maturation. AECA binding to endothelial cells would cause endothelial activation or damage, with proinflammatory cytokine release, fostering a hypercoagulable state by leukocyte activation by proinflammatory cytokines. This, in turn, would lead to coronary artery lesions. KD vasculitis might be initiated upon AECA binding to the vasa vasorum and progress to panvasculitis and a vulnerable vessel wall, resulting in an aneurysm. The aneurysm would cause flow recirculation and alteration of wall shear stress. Consequently, platelets activated by shear stress, along with ultra-large von Willebrand factor (VWF) released by endothelial cells, would cause platelet-driven arterial thrombosis. Autoimmunity-associated thrombosis initiated by AECA binding to endothelial cells might play a major role in the pathogenesis of certain subtypes of KD. The notion of KD consisting of subtypes, the major one of which is AECA-associated vasculitis, will help facilitate a better understanding of KD and further promote early and accurate diagnosis, which remains challenging.

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Section: Autoimmunothrombosis In Kdmentioning

confidence: 99%

Autoimmune Aspects of Kawasaki Disease

Sakurai¹

2019

J Investig Allergol Clin Immunol

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“…Treatment with ET-1 receptor blockers has been found effective in PAH and digital ulcer prevention in SSc 53. Interestingly, in in vitro studies incubation of HUVECs with AECA-positive sera from patients with SLE and pre-eclampsia resulted in enhanced release of ET-1 54 55. Whether this is also true for sera from AECA-positive patients with SSc, however, needs to be demonstrated.…”

Section: Pathogenic Role Of Aeca In Sscmentioning

confidence: 99%

Anti-endothelial cell antibodies in systemic sclerosis

Mihai

Tervaert

2010

Ann Rheum Dis

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Anti-endothelial cell antibodies (AECA) are a heterogeneous class of antibodies whose role in the pathogenesis of autoimmune diseases with vascular involvement has been extensively studied. Systemic sclerosis (SSc) is one of the systemic autoimmune diseases in which endothelial dysfunction is well defined and important in the development of the disease. AECA are present in the serum samples of many patients with SSc. Depending on the detection method and on patient selection, 22-86% of patients test positive for AECA. Among the demonstrated clinical associations, lung and peripheral vascular involvement are the most common. In this paper, the methods of detection, various molecular specificities and the possible pathogenic mechanisms of AECA in SSc are reviewed.

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“…In other words, the relationship between hypertension, cerebral hemorrhage and infarction is complex. Furthermore, studies have suggested immune system involvement in pregnancy hypertension [38][39][40][41], but not in essential hypertension.…”

Section: Pih Susceptibility Genesmentioning

confidence: 99%

Comparison between Essential Hypertension and Pregnancy-induced Hypertension: a Genetic Perspective

Nakayama

Yamamoto

2009

Endocr J

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Abstract. Essential hypertension (EH) accounts for 80-90% of hypertension, and pregnancy-induced hypertension (PIH) is responsible for hypertension during pregnancy. Both considered multifactorial disorders. While both have many features in common, conditions and causes of these diseases have yet to be clarified. Since both diseases are associated with hypertension, the genetic backgrounds may contain common features. The present study reviewed similarities and differences between women with EH and PIH, with a particular focus on their genetic backgrounds.

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Effects of anti‐endothelial cell antibody in pre‐eclampsia on endothelin‐1 release from cultured endothelial cells

Cited by 16 publications

References 21 publications

Autoimmune Aspects of Kawasaki Disease

Autoimmune Aspects of Kawasaki Disease

Anti-endothelial cell antibodies in systemic sclerosis

Comparison between Essential Hypertension and Pregnancy-induced Hypertension: a Genetic Perspective

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