Abstract
We read with interest the report by Bonet et al. (1) of an effect of oxidized LDL on placental trophoblast and macrophage functions. We would like to complement their data with recent information regarding B2-glycoprotein I (B2-GPI), a normal plasma component that has been found to be also synthesized by the placental trophoblast (2). B2-GPI has been shown to bind copper-oxidized plasma lipoproteins and inhibit the in vitro uptake by murine macrophage cells (3).
B2-GPI has an important role in the maintenance of blood fluidity by possessing anticoagulant activity (4). Recently, it was demonstrated that, compared with native LDL, oxidized LDL can increase thrombin generation 12-fold by providing a supporting surface for the assembly of the prothrombinase complex (5). The ability of B2-GPI to bind oxidized LDL may be another aspect of its antithrombotic mechanism, and may prevent placental ischemia and dysfunction during pregnancy. It would therefore be of interest to determine whether B2-GPI also has a modulating effect on the cytotoxicity of oxidized LDL, as described Bonet and colleagues.
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