PMID- 10736236
OWN - NLM
STAT- MEDLINE
DCOM- 20000525
LR  - 20091103
IS  - 0143-4004 (Print)
IS  - 0143-4004 (Linking)
VI  - 21
IP  - 2-3
DP  - 2000 Mar-Apr
TI  - Normal expression of cell adhesion molecules in placentae from women with 
      systemic lupus erythematosus and the antiphospholipid syndrome.
PG  - 142-9
AB  - Pregnant women with active systemic lupus erythematosus (SLE) and/or the 
      antiphospholipid syndrome (APS) are prone to recurrent miscarriage, 
      pre-eclampsia, intrauterine growth restriction and premature delivery. Placental 
      dysfunction may account for these complications yet the mechanisms remain 
      uncertain. Amongst these, an inflammatory response in the placental vasculature 
      could play a role, involving recruitment of neutrophils and platelets and the 
      increased endothelial expression of cell adhesion molecules (CAM), central to the 
      recruitment process. The aim of this study was primarily to investigate CAM 
      expression in the fetoplacental vasculature in women with SLE/APS. Circulating 
      maternal concentrations of soluble CAM were also elucidated. There were no 
      differences in CAM immunostaining in placentae from patients with SLE and/or APS 
      compared with controls. In both patients and controls moderate immunostaining for 
      the intercellular adhesion molecule-1 (ICAM-1) was observed in placental vascular 
      endothelium and mild immunostaining was present in the placental villous stroma. 
      Strong immunostaining for platelet endothelial CAM (PECAM) occured in the 
      placental vascular endothelium whereas P-selectin was mildly expressed in the 
      stem vessel endothelium only. Vascular CAM-1 (VCAM-1) and E-selectin were 
      undetectable in either study or control placentae. In contrast, ICAM-1 and VCAM-1 
      but not E-selectin, as assessed by immunoassay (ELISA), were elevated in maternal 
      serum from SLE/APS patients compared with controls. This study suggests that 
      upregulation of CAM expression and subsequent activation of neutrophil and/or 
      platelet activity within the placental villous tree is unlikely to be a mechanism 
      by which the adverse pregnancy outcome arises in SLE/APS pregnancies. However, 
      maternal endothelial cell activation (ECA) may play a more important role.
CI  - Copyright 2000 Harcourt Publishers Ltd.
FAU - Lakasing, L
AU  - Lakasing L
AD  - Fetal Health Laboratory, Division of Obstetrics and Gynaecology, Guy's, King's 
      and St Thomas' School of Medicine (GKT), London, SE1, UK.
FAU - Campa, J S
AU  - Campa JS
FAU - Parmar, K
AU  - Parmar K
FAU - Poston, R
AU  - Poston R
FAU - Hunt, B J
AU  - Hunt BJ
FAU - Poston, L
AU  - Poston L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Placenta
JT  - Placenta
JID - 8006349
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (E-Selectin)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Adult
MH  - Antiphospholipid Syndrome/*complications/*immunology
MH  - Case-Control Studies
MH  - Cell Adhesion Molecules/*metabolism
MH  - E-Selectin/metabolism
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Lupus Erythematosus, Systemic/*complications/*immunology
MH  - Placenta/*immunology
MH  - Pregnancy
MH  - Pregnancy Complications/*immunology
MH  - Vascular Cell Adhesion Molecule-1/metabolism
EDAT- 2000/03/29 09:00
MHDA- 2000/06/08 09:00
CRDT- 2000/03/29 09:00
PHST- 2000/03/29 09:00 [pubmed]
PHST- 2000/06/08 09:00 [medline]
PHST- 2000/03/29 09:00 [entrez]
AID - S0143400499904782 [pii]
AID - 10.1053/plac.1999.0478 [doi]
PST - ppublish
SO  - Placenta. 2000 Mar-Apr;21(2-3):142-9. doi: 10.1053/plac.1999.0478.