Phospholipid binding of antiphospholipid antibodies and placental anticoagulant protein.
Lisa R. Sammaritano,Azzudin E. Gharavi,Consolacion Soberano,Roger A. Levy,Michael D. Lockshin +4 more
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TL;DR: Data support the hypotheses that aPL and PAP I may recognize similar phospholipid epitopes and that in vivo interaction may occur and interact additively in anticoagulant activity inin vitro clotting systems.
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Abstract: We evaluated the interaction of antiphospholipid antibodies (aPL) with placental anticoagulant protein I (PAP I), a calcium-dependent phospholipid binding protein which may act as a natural anticoagulant. Clotting assays showed additive prolongation of clotting times with aPL and PAP I. ELISA and vesicle phospholipid binding studies showed PAP I inhibition of aPL binding to phospholipid but no inhibition of PAP I-phospholipid binding by aPL. aPL and PAP I interact additively in anticoagulant activity inin vitro clotting systems and compete for phospholipid in ELISA system. These data support the hypotheses that aPL and PAP I may recognize similar phospholipid epitopes and thatin vivo interaction may occur.
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Citations
Pregnancy Loss in the Antiphospholipid-Antibody Syndrome — A Possible Thrombogenic Mechanism
Jacob H. Rand,Xiao-Xuan Wu,Harry A.M. Andree,Charles J. Lockwood,Seth Guller,Jonathan Scher,Peter C. Harpel +6 more
TL;DR: Antiphospholipid antibodies reduce the levels of annexin V and accelerate the coagulation of plasma on cultured trophoblasts and endothelial cells and how they affect the procoagulant activity of these cells is studied.
537
Activation of cultured vascular endothelial cells by antiphospholipid antibodies.
Ronit Simantov,Johanna M. LaSala,Siu K. Lo,Azzudin E. Gharavi,Lisa R. Sammaritano,Jane E. Salmon,Roy L. Silverstein +6 more
TL;DR: The hypothesis that circulating antiphospholipid antibodies (aPL) activate vascular endothelial cells, thereby leading to a pro-thrombotic state is supported.
Heart Valve Involvement (Libman-Sacks Endocarditis) in the Antiphospholipid Syndrome
TL;DR: Current data suggest a role for aPLs in the pathogenesis of valvular lesions, as indicated by the finding of subendothelial deposits of immunoglobulins, including anticardiolipin antibodies, and of colocalized complement components in deformed valves from patients with APS.
441
Hydroxychloroquine directly reduces the binding of antiphospholipid antibody–β2-glycoprotein I complexes to phospholipid bilayers
Jacob H. Rand,Xiao-Xuan Wu,Anthony S. Quinn,Pojen P. Chen,James J. Hathcock,Douglas J. Taatjes +5 more
TL;DR: The results support the possibility that HCQ, or analogous molecules, may offer novel nonanticoagulant therapeutic strategies for treating APS and reduce the formation of aPL-beta2GPI complexes to phospholipid bilayers and cells.
219
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