Co-purification of arrestin like proteins with alpha-enolase from bovine myocardial tissues and the possible role in heart diseases as an autoantigen

Mirshahi, Massoud; Marchand, Sylvie

doi:10.1016/j.bbrc.2015.03.086

Cited by 3 publications

(4 citation statements)

References 27 publications

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“…Translocation of ENO1 to the cell surface can drive the production of specific ENO1 autoantibodies, causing autoimmune diseases. In the infarcted heart, β-arrestin associates with ENO1 and translocates together to the cell membrane as auto-antigens, thus inducing high levels of anti-ENO1 and anti-arrestin antibodies in patients' sera [27]. We confirmed the co-expression of ENO1 and β-arrestin in EVT in the first trimester placenta of uRM patients (Fig.…”

Section: Discussionsupporting

confidence: 72%

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Anti α-enolase antibody is a novel autoimmune biomarker for unexplained recurrent miscarriages

et al. 2019

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Background We recently demonstrated the increased abundance of anti-trophoblast antibodies (ATAB) in sera of patients with unexplained recurrent miscarriages (uRM). Further, the ATAB-positive sera bound to JEG-3 human choriocarcinoma cells in vitro, resulting in decreased productions of β-human chorionic gonadotropin (β-hCG) and progesterone in these cells. However, the specific antigenic epitopes of ATAB have remained unknown. Therefore, it was the aim of this study to determine specific targets of ATAB in uRM patients. Methods Potential targets of ATAB were analyzed by 2-dimensional difference gel electrophoresis (2D-DIGE) and mass spectrometry, and thereby identifying α-Enolase (ENO1). ATAB targeting of ENO1 was further confirmed in a competitive binding assay. Levels of anti-ENO1 antibodies as well as β-hCG and progesterone were quantified with enzyme-linked immunosorbent assay (ELISA). Additionally, expression of ENO1 was analyzed in first trimester placentas by immunohistochemistry and immunofluorescence analysis. Findings We here identified ENO1 as a prominent target of ATAB. Serum levels of anti-ENO1 antibodies were increased in ATAB-positive compared to ATAB-negative patients. Further, increased expression of ENO1 and its co-expression with β-arrestin was found in the extra villous trophoblasts of uRM patients in first trimester placentas. In vitro, anti-ENO1 antibodies decreased the secretion of β-hCG and progesterone in JEG-3 and primary human villous trophoblast cells. Interpretation Serum anti-ENO1 antibodies might be an autoimmune biomarker for uRM. Targeting the formation of anti-ENO1 antibodies or inhibition of ENO1 expression could potentially represent therapeutic strategies for these patients. Fund All authors declare no conflict of interest. Yao Ye was supported by the China Scholarship Council. Hellen Ishikawa-Ankerhold and Christian Schulz were supported by the SFB914, projects Z01 and A10. None of the rest authors has any conflict of interest to declare.

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Section: Discussionsupporting

confidence: 72%

“…9). β-arrestin plays a role in G-protein receptor desensitization, receptor endocytosis, activation of extracellular signal regulated kinases and other mitogen activated protein kinases [27]. ENO1 can also be translocated to the cell surface by extracellular peptidyl arginine deiminase [20] and lipopolysaccharides [28].…”

Section: Discussionmentioning

confidence: 99%

Anti α-enolase antibody is a novel autoimmune biomarker for unexplained recurrent miscarriages

et al. 2019

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“…These findings may explain an occasional detection of anti-enolase and anti-arrestin AAbs in the same patient with CAR or MS, suggesting that such complexes could be released from damaged photoreceptor cells, then processed by antigen-presenting cells (38, 47). Surprisingly, AAbs against arrestin and α-enolase were also reported in some patients with coronary heart disease (48). When investigators exposed cardiomyocytes to monoclonal antibody against arrestin or enolase in vitro , they observed decreased cell proliferation, suggesting that antibodies bound to the membrane-exposed epitopes of arrestin and enolase in living cells (48).…”

Section: Enolasementioning

confidence: 99%

“…Surprisingly, AAbs against arrestin and α-enolase were also reported in some patients with coronary heart disease (48). When investigators exposed cardiomyocytes to monoclonal antibody against arrestin or enolase in vitro , they observed decreased cell proliferation, suggesting that antibodies bound to the membrane-exposed epitopes of arrestin and enolase in living cells (48). The study suggested that these AAbs may be involved in the induction of cardiac autoimmune diseases.…”

Section: Enolasementioning

confidence: 99%

Impact of Autoantibodies against Glycolytic Enzymes on Pathogenicity of Autoimmune Retinopathy and Other Autoimmune Disorders

Adamus

2017

Front. Immunol.

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Autoantibodies (AAbs) against glycolytic enzymes: aldolase, α-enolase, glyceraldehyde-3-phosphate dehydrogenase, and pyruvate kinase are prevalent in sera of patients with blinding retinal diseases, such as paraneoplastic [cancer-associated retinopathy (CAR)] and non-paraneoplastic autoimmune retinopathies, as well as in many other autoimmune diseases. CAR is a degenerative disease of the retina characterized by sudden vision loss in patients with cancer and serum anti-retinal AAbs. In this review, we discuss the widespread serum presence of anti-glycolytic enzyme AAbs and their significance in autoimmune diseases. There are multiple mechanisms responsible for antibody generation, including the innate anti-microbial response, anti-tumor response, or autoimmune response against released self-antigens from damaged, inflamed tissue. AAbs against enolase, GADPH, and aldolase exist in a single patient in elevated titers, suggesting their participation in pathogenicity. The lack of restriction of AAbs to one disease may be related to an increased expression of glycolytic enzymes in various metabolically active tissues that triggers an autoimmune response and generation of AAbs with the same specificity in several chronic and autoimmune conditions. In CAR, the importance of serum anti-glycolytic enzyme AAbs had been previously dismissed, but the retina may be without pathological consequence until a failure of the blood–retinal barrier function, which would then allow pathogenic AAbs access to their retinal targets, ultimately leading to damaging effects.

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Anti-Trophoblast-Antikörper, ihre Identifikation, Wirkmechanismen und mögliche Behandlung

Jeschke,

Rogenhofer,

Thaler

et al. 2023

Reproduktionsimmunologie

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Co-purification of arrestin like proteins with alpha-enolase from bovine myocardial tissues and the possible role in heart diseases as an autoantigen

Abstract: We suggest a possible interaction between ALP and alpha-enolases yielding a complex that may be involved in the induction of cardiac autoimmune diseases.

Cited by 3 publications

References 27 publications

Anti α-enolase antibody is a novel autoimmune biomarker for unexplained recurrent miscarriages

Anti α-enolase antibody is a novel autoimmune biomarker for unexplained recurrent miscarriages

Impact of Autoantibodies against Glycolytic Enzymes on Pathogenicity of Autoimmune Retinopathy and Other Autoimmune Disorders

Anti-Trophoblast-Antikörper, ihre Identifikation, Wirkmechanismen und mögliche Behandlung

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