title: Pre-eclampsia does not change the adhesion molecule status in the placental bed.
abstract: During normal placentation trophoblast cells invade maternal tissues and remodel the uterine arteries into low-resistance channels. In pre-eclampsia, trophoblast invasion is impaired and this, along with endothelial dysfunction, has been suggested to play a role in the pathogenesis of pre-eclampsia. We studied the expression of adhesion molecules important for leukocyte extravasation in the placental bed with immunohistochemistry and compared the expression in pre-eclampsia to that in normal pregnancy. Our major finding was that only invasive trophoblasts expressed cutaneous lymphocyte antigen-1 (CLA-1) in the third trimester of pregnancy, whereas villous trophoblasts did not. In the first trimester both villous trophoblasts and invasive trophoblast cells in decidua remained negative for CLA-1. Pre-eclampsia did not change the expression of leukocyte-endothelium adhesion or lymphocyte homing-associated antigens, ICAM-1, ICAM-2, VCAM, P-selectin, E-selectin, L-selectin, CLA-1, CD73, VAP-1 and alphaEbeta7 in the placental bed. Furthermore, pre-eclampsia was not associated with an aberrant accumulation of lymphocytes carrying antigens of any particular known organ-specific homing systems. The results on the unchanged pattern of adhesion molecule expression in pre-eclampsia suggests that there is no major change in the adhesive properties of the endothelium of the placental bed in pre-eclampsia.
authors.affiliation: National Public Health Institute and MediCity Research Laboratory, University of Turku, Tykistökatu 6 a, Turku, FIN-20520, Finland.
authors.forename: K
authors.initials: K
authors.lastname: Jaakkola
authors.forename: V
authors.initials: V
authors.lastname: Jokimaa
authors.forename: M
authors.initials: M
authors.lastname: Kallajoki
authors.forename: S
authors.initials: S
authors.lastname: Jalkanen
authors.forename: E
authors.initials: E
authors.lastname: Ekholm
mesh_terms: D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000276:immunology / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008214:Lymphocytes / Q000276:immunology / Q000473:pathology; D008562:Membrane Glycoproteins / Q000378:metabolism; D010920:Placenta / Q000276:immunology* / Q000473:pathology; D011225:Pre-Eclampsia / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D011247:Pregnancy; D014327:Trophoblasts / Q000276:immunology / Q000473:pathology
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; C063419:CTAGE1 protein, human; D015815:Cell Adhesion Molecules; D008562:Membrane Glycoproteins