title: Expression of cell adhesion molecules in the extravillous trophoblast is altered in IUGR.
abstract: OBJECTIVE
  The invasion of trophoblast cells into the uterine wall and its arterial system is essential for the normal development of pregnancy. Cell adhesion molecules (CAM), such as the immunoglobulin superfamily and integrins, play a crucial role in a number of immunological reactions and in the invasion of the human trophoblast. Intrauterine growth restriction (IUGR) has been associated with abnormal trophoblast invasion. Therefore, the expression of CAM in the extravillous trophoblast of pregnancies complicated by IUGR might be different from normal pregnancies.
  
  
  METHODS
  Normal (n = 21) and IUGR (n = 19) placentas were collected and stored at -70 degrees C. Immunohistochemistry (avidin-biotin complex peroxidase-doublestaining) of frozen tissue sections was performed using antibodies specific for the immunoglobulin superfamily vascular adhesion molecule-1 (VCAM-1; CD 106), intercellular adhesion molecule (ICAM-1) (CD 54), ICAM-2 (CD 102), ICAM-3 (CD 50), the integrins alpha 2 beta 1, alpha 3 beta 1, alpha 4 beta 1, alpha 5 beta 1, alpha 6 beta 1 and cytokeratin. The percentage of immunopositive extravillous trophoblast cells (EVT) and the intensity of the immunoreactivity for the various CAM and integrin antibodies was assessed.
  
  
  RESULTS
  In IUGR placentas, there was less expression of VCAM-1 (CD 106), alpha 2 beta 1, alpha 3 beta 1, and alpha 5 beta 1 (P < 0.05) in the extravillous trophoblast than in normal pregnancies. Finally we observed for the first time that ICAM-3 was expressed on EVT and that its expression was markedly up-regulated in the EVT or IUGR placentas. No differences were found for ICAM-1 (CD 54), ICAM-2 (CD 102), alpha 4 beta 1 and alpha 6 beta 1.
  
  
  CONCLUSIONS
  Our data show that there are significant differences in the expression of cell adhesion molecules of the extravillous trophoblast from IUGR and normal pregnancies. These differences might reflect changes in the immunological reactions and cell-cell interactions between mother and the developing fetus which could interfere with fetal growth.
authors.affiliation: Department of Obstetrics & Gynecology, University of Giessen, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Zygmunt
authors.forename: B
authors.initials: B
authors.lastname: Boving
authors.forename: J
authors.initials: J
authors.lastname: Wienhard
authors.forename: K
authors.initials: K
authors.lastname: Münstedt
authors.forename: G
authors.initials: G
authors.lastname: Braems
authors.forename: R M
authors.initials: RM
authors.lastname: Bohle
authors.forename: U
authors.initials: U
authors.lastname: Lang
mesh_terms: D015703:Antigens, CD; D000943:Antigens, Differentiation; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D005260:Female; D005317:Fetal Growth Retardation / Q000276:immunology*; D006801:Humans; D007150:Immunohistochemistry; D007231:Infant, Newborn; D016023:Integrins / Q000378:metabolism; D011247:Pregnancy; D014327:Trophoblasts / Q000276:immunology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D000943:Antigens, Differentiation; D015815:Cell Adhesion Molecules; C483616:ICAM3 protein, human; D016023:Integrins; D019010:Vascular Cell Adhesion Molecule-1