Annexin A2 autoantibodies in thrombosis and autoimmune diseases

Cañas, Felipe; Simonin, Laurent; Couturaud, Francis; Renaudineau, Yves

doi:10.1016/j.thromres.2014.11.034

Cited by 45 publications

(34 citation statements)

References 74 publications

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“…It was shown that AnxA2 interacts with β2GPI and Toll-like receptor 4 (TLR4) in a signalling complex leading to an inflammatory and pro-coagulant phenotype on endothelial cells ( 20 , 21 ). Autoantibodies against AnxA2 were detected in APS patients, but the diagnostic sensitivity of the AnxA2 test is quite low, and AnxA2 autoantibodies were also detected in patients suffering from other autoimmune conditions lowering also the diagnostic specificity ( 8 ).…”

Section: Discussionmentioning

confidence: 99%

Detection of multiple annexin autoantibodies in a patient with recurrent miscarriages, fulminant stroke and seronegative antiphospholipid syndrome

et al. 2016

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Anti-phospholipid syndrome (APS) is one of the main causes for recurrent miscarriages. The diagnosis of APS is based on the occurrence of clinical symptoms such as thrombotic events or obstetric complications as well as the detection of antiphospholipid antibodies directed against β2-glycoprotein I and cardiolipin, or a positive lupus anticoagulant assay. However, there is a subpopulation of patients with clinical symptoms of APS, but the lack of serological markers (seronegative APS). In addition, a large proportion of patients with unexplained recurrent miscarriages exist. These cases may be attributed, at least in part, to a seronegative APS. The presence of autoantibodies against annexins is potentially associated with APS. Here we used immunoassays and immunoblots to detect autoantibodies directed against annexin A1-5, and A8, respectively, in a patient with a seronegative APS and a history of six recurrent pregnancy losses and fulminant stroke. We found strong IgM isotype antibody reactivity directed against annexin A2 and annexin A8, and moderate to weak IgM isotype antibody reactivity directed against annexin A1, A3, and A5. Further studies will evaluate the diagnostic value of IgM isotype antibodies against annexin A1-A5, and A8 for seronegative APS and recurrent miscarriages.

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Section: Discussionmentioning

confidence: 99%

Detection of multiple annexin autoantibodies in a patient with recurrent miscarriages, fulminant stroke and seronegative antiphospholipid syndrome

et al. 2016

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“…Moreover, in patients with antibiotic‐refractory LA, the levels of anti‐ECGF autoantibodies correlated with obliterative microvascular lesions in synovial tissue, suggesting that these antibodies may have pathologic potential . Antibody responses to ECGF were not found in patients with other types of arthritis, and reactivity with MMP‐10 and Apo B‐100 were unusual in other arthritides; however, annexin A2 antibody responses occur in several rheumatic diseases .…”

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confidence: 99%

Autoimmune Arthritides, Rheumatoid Arthritis, Psoriatic Arthritis, or Peripheral Spondyloarthritis Following Lyme Disease

Arvikar

Crowley

Sulka

et al. 2016

Arthritis & Rheumatology

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Objective To describe systemic autoimmune joint diseases following Lyme disease and to compare their clinical features with Lyme arthritis. Methods Records of all adult patients referred to our Lyme arthritis clinic over a 13-year period in whom we diagnosed a systemic autoimmune joint disease following Lyme disease were reviewed. For comparison, records of patients enrolled in our Lyme arthritis (LA) cohort over the most recent 2-year period were analyzed. IgG antibodies to Borrelia burgdorferi and to 3 Lyme disease-associated autoantigens were measured. Results We identified 30 patients who developed a new-onset systemic autoimmune joint disorder a median of 4 months after Lyme disease, usually erythema migrans (EM). Fifteen had rheumatoid arthritis (RA), 13 had psoriatic arthritis (PsA), and 2 had peripheral spondyloarthropathy (SpA). The 30 patients typically had polyarthritis; and those with PsA/SpA often had previous psoriasis, axial involvement, or enthesitis. In the comparison group of 43 LA patients, monoarticular knee arthritis, without prior EM, was the usual clinical picture. Most systemic autoimmune patients had positive tests for B. burgdorferi IgG antibodies by ELISA, but they had significantly lower titers and lower frequencies of Lyme-associated autoantibodies than LA patients. Prior to our evaluation, the patients often received additional antibiotics for presumed Lyme arthritis without benefit. We prescribed anti-inflammatory therapies, most commonly disease modifying anti-rheumatic drugs (DMARDs), resulting in improvement. Conclusion Systemic autoimmune joint diseases, RA, PsA/SpA, may follow Lyme disease. Development of polyarthritis after antibiotic-treated erythema migrans, previous psoriasis, or low-titer B. burgdorferi antibodies are clues to the correct diagnosis.

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“…Mice deficient in AnxA2 display increased fibrin accumulation within blood vessels and impaired clearance of injury-induced thrombi (24). Anti-AnxA2 auto-antibodies have been reported in patients with thrombosis-associated diseases, such as antiphospholipid syndrome, pre-eclampsia and cerebral venous thrombosis (38). On the other hand, overexpression of AnxA2 in acute promyelocytic leukemia patients leads to a bleeding diathesis due to excessive cell surface AnxA2-dependent generation of plasmin (39).…”

Section: Discussionmentioning

confidence: 99%

EPAC1 regulates endothelial Annexin A2 cell surface translocation and plasminogen activation

Mei

Cheng

2017

Preprint

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Annexins, a family of highly conserved calcium-and phospholipid-binding proteins, play important roles in a wide range of physiological functions. Among the twelve known annexins in human, Annexin A2 (AnxA2) is one of the most extensively studied and has been implicated in various human diseases. AnxA2 can exist as a monomer or a heterotetrameric complex with S100A10 (P11) and plays a critical role in many cellular processes including exocytosis/endocytosis and membrane organization. At the endothelial cell surface, (AnxA2•P11)2 tetramer, acting as a coreceptor for plasminogen and tissue plasminogen activator (t-PA), accelerates t-PA dependent activation of the fibrinolytic protease, plasmin, the enzyme responsible for thrombus dissolution and degradation of fibrin. This study shows that exchange proteins directly activated by cAMP isoform 1 (EPAC1) interacts with AnxA2 and regulates its biological functions by modulating its membrane translocation in endothelial cells. Using genetic and pharmacological approaches, it is demonstrated that EPAC1, acting through the PLCε-PKC pathway, inhibits AnxA2 surface translocation and plasminogen activation. These results suggest that EPAC1 plays a role in the regulation of fibrinolysis in endothelial cells and may represent a novel therapeutic target for disorders of fibrinolysis.

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Annexin A2 autoantibodies in thrombosis and autoimmune diseases

Cited by 45 publications

References 74 publications

Detection of multiple annexin autoantibodies in a patient with recurrent miscarriages, fulminant stroke and seronegative antiphospholipid syndrome

Detection of multiple annexin autoantibodies in a patient with recurrent miscarriages, fulminant stroke and seronegative antiphospholipid syndrome

Autoimmune Arthritides, Rheumatoid Arthritis, Psoriatic Arthritis, or Peripheral Spondyloarthritis Following Lyme Disease

EPAC1 regulates endothelial Annexin A2 cell surface translocation and plasminogen activation

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