Ontogeny of beta 2 glycoprotein I and annexin V in villous placenta of normal and antiphospholipid syndrome pregnancies

beta(2)-glycoprotein I (beta(2)GPI) and annexin V (AV) have been implicated in the pathophysiology of the antiphospholipid syndrome (APS). We investig ated their placental expression in normal villous tissues throughout gestat ion; first trimester n = 10, early second trimester; n = 4, preterm: n = 5) and term; n = 7 and in APS (2 first trimester, 1 preterm and 8 term delive ries). beta(2)GPI and AV were both expressed by the placenta from as early as seven weeks gestation and were colocalised to the syncytiotrophoblast. b eta(2)GPI staining was also observed in stromal cells: being present in pha gocytic Hofbauer cells and surrounding newly formed fetal vessels in a peri vascular pattern, from seven to seventeen weeks gestation. An abnormal morp hological distribution of AV was noted in one first trimester APS placenta, and for beta(2)GPI in a further first trimester placenta. When placental p roteins were extracted from villous tissue, the concentration of AV/mg prot ein in term APS placentas (median, interquartile range) (aPS; 8.16, 7.87-9. 72 mu g/mg) was significantly higher (p <0.005) than normal term levels (no rmal; 2.47, 2.28-2.54 mu g/mg). beta(2)GPI increased with advancing gestati on (first trimester; 0.93, 0.64-1.26 mu g/mg, term; 3.67, 2.58-4.48 mu g/mg ) in normal pregnancy. Term APS placentas had a reduced beta(2)GPI content (2.31. 1.87-2.49 mu g/mg), p <0.05. The placental role of these proteins re mains to be identified.