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Antiphospholipid syndrome and tissue factor: a thrombotic coupleResearch Unit and Rheumatology Department, Reina Sofia Hospital, Córdoba, Spain, rosario.lopez.exts{at}juntadeandalucia.es
Research Unit and Rheumatology Department, Reina Sofia Hospital, Córdoba, Spain
Research Unit and Rheumatology Department, Reina Sofia Hospital, Córdoba, Spain
Research Unit and Rheumatology Department, Reina Sofia Hospital, Córdoba, Spain
Lupus Research Unit, St Thomas Hospital, London, UK
The antiphospholipid syndrome (APS) is characterized by thrombosis and/or pregnancy morbidity in the presence of antiphospholipid antibodies (aPL). Among the thrombogenic mechanisms proposed, it has been suggested that aPL can stimulate tissue factor (TF) expression by endothelial cells (ECs) and monocytes. Moreover, our in vivo studies have shown that APS patients (particularly those with thrombosis) have increased monocyte TF expression. Yet, the molecular mechanism(s) by which aPL induce TF expression has not been completely underscored. In a recent study, we have demonstrated that aPL induces TF expression in monocytes from APS patients by activating, simultaneously and independently, the phosphorylation of MEK-1/ERK proteins, and the p38 MAP kinase-depenent nuclear translocation and activation of NF
Key Words: intracellular signalling • monocyte tissue factor expression • thrombosis in APS
Lupus, Vol. 15, No. 3,
161-166 (2006) This article has been cited by other articles:
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B/Rel proteins. Understanding the intracellular mechanism(s) of aPL-mediated monocyte activation may help to establish new therapeutic approaches, such as selective inhibition of MAP kinases, to reverse the prothrombotic state in APS. Furthermore, the contribution of TF to a protrombotic state in the APS provides a renewed focus on antithrombotic therapies in current use, including the oral anticoagulation and, more recently, the use of statins, which have been proven to be effective in the inhibition of EC and monocyte TF-expression. 
