Monoclonal Antiphospholipid antibody reactivity against human first-trimester placental trophoblasts

A.37

Abstracts: 1.M.W.P.A. Australia 1994 ON

FACTORS

CONTROLLING

ANGIGGENESIS

IN THE

HUMAN TERM PLACENTA: THE

SIGNIFICANCE OF CHANGES IN FETAL PERFUSIONPRESSURE.A.L. Kuimtt Dcpartmcnt of Anatomy, University of Cambriigc, UK.

and GJ. Burton

Theobjective of the study was IO detcrminc the cffccts of mrchartical factors on a&hclii

proliiaatiat in the human placcnrrl villour vasculaturc. In order to rhicvo this aim. cxpcrimenta were c&ad out bt which individual fctsl lobules were pcrfuscd with tissue culture medium nt two diflarmnt sudud pmmms (40 and 100 mm Hg rcopectivcly). The perfused area wu thc.nremoved utd diced Into small bIocks whioh were quench-frozen in liquid nitrogen. Ctyostat sections were then obwincd utd fixed In acctottc at 4 ‘C. Proliferating ccl1 nuclear antigen wss then idcntiftcd using Ki67 antibody as 8 marker. The number of proliferating nuclei per villous profile was scorai using a light microscope and canpuirpl made between the IWO pressure groups. The results showed thst there wcrc more proliferating cndolhrlial nuclei at the higher prcssurc of 100 mm Hg relative to the pressure of 40 mm Hg. 1.96 SEM 0.18 and 0.86 SEM 0.11 rqrectivcly. and this was statistically significant (p c 0.05). On the other hand. them was no rignif@ant diffcratcc in the number of Welled cytotrophoblasticnuclei bctwccn the two pusttre groups 0.27 SRM 0.06 md 03 Sw( 0.06 respectively. p > 0.05. This provided a positive control that the Welling cff&rtcy of the pimaty antibody was similar in the two series. ‘It is therefore concluded thst mechanicsI fstors may play a role in villous sngiogcncsisand the formation of terminal villi.

ANTIPHOSPHOLIPID ANTIBODY REACIIVITY AGAlNST HUMAN FIRST-TRIMESTER PLACENTAL TROPHOBLASTS. Hiroshi Katsuragawa’, Neal S. Rote*, Hideharu Kanzaki, Takuya Inoue, Shinji Narukawa and Takahide Mori, Department of Gynecology and Obstetrics’, Faculty of Medicine, Kyoto University, Kyoto, 606, Japan, Department of Microbiology and Immunology and Obstetrics and Gynecology, School of Medicine, Wright State University, Dayton, Ohio, 45435 U.S.A.* MONOCLONAL

The antiphospholipid antibody syndrome is characterized by apparent placental damage in the first trimester resulting in pregnancy loss or severe intrauterine growth retardation. In order to investigate the binding of antibodies against negatively charged phospholipids (aPLs) to human first-trimester placenta we tested the reactivity of three mouse monoclonal aPLs against formalin fixed and frozen sections of firsttrimester placentae by staining by immunoperoxidase. Each monoclonal antibody reacted differently with cardiolipin (CL) and phosphatidylserine (PS); 3SB9b reacted with PS (CL-/PS+), Dl lA4 reacted with CL (CL+/PS-), and BA3B5C4 reacted with both CL and PS (CL+/PS+). 3SB9b reacted strongly with the syncytiotrophoblastic layer of both formalin and frozen placental tissue. Sporadic reactivity was observed against the cytotrophoblastic layer. BA3BX4 reacted strongly and specifically with cytotrophoblastic cells. DllA4 reacted minimally or, more commonly, not at all. The trophoblastic layer in the first trimester placenta directly in contact with the maternal circulation is most reactive with aPLs that are PS+ rather than CL+, suggesting that the trophoblasts may potentially be directly damaged through mechanisms unrelated to thrombosis. In addition, the differential reactivity of 3SB9b and BA3B5C4 suggests that the antigenic conformation involving PS on the cytotrophoblast is altered concurrent with fusion into the syncytium.