title: Human first-trimester placenta intra-arterial trophoblast cells express the neural cell adhesion molecule.
abstract: The supposed influence of endometrial natural killer (NK) cells on the trophoblast invasion activities especially on intravasation of uteroplacental arteries in the non-pathogenic human first-trimester placenta was studied by means of immunohistochemistry. To identify extravillous trophoblast cells, smooth muscle cells, endothelia, endometrial glands, decidual stroma cells and endometrial NK cells, antibodies against cytokeratins, vimentin, smooth muscle cells, epithelium specific antigen and endothelial cells were employed. Furthermore, the immunohistochemical distribution patterns of CD56, CD57 and CD94 were studied and compared with the localization of invading trophoblast cells. Remodelling and dilatation of uteroplacental arteries starts before trophoblast cells can be found in the vicinity of the vessels. Nevertheless, subsequent trophoblast invasion of the arterial wall will lead to media destruction and intravasation only on focally restricted areas. This process is accompanied by the disappearance of endothelial cells and the immediate expression of the neural cell adhesion molecule (N-CAM, CD56) by intra-arterial trophoblast cells, which are eventually beginning to form intraluminal plugs. These findings led us to the conclusion that in the human pregnancy-induced physiological changes of the uteroplacental blood flow and the peripheral blood NK cell activity is not only, but also, due to the effect of CD56 expression by intra-arterial trophoblast cells.
authors.affiliation: Institut für Histologie und Embryologie, Universität Graz, Austria.
authors.forename: J
authors.initials: J
authors.lastname: Pröll
authors.forename: A
authors.initials: A
authors.lastname: Blaschitz
authors.forename: M
authors.initials: M
authors.lastname: Hartmann
authors.forename: J
authors.initials: J
authors.lastname: Thalhamer
authors.forename: G
authors.initials: G
authors.lastname: Dohr
mesh_terms: D000911:Antibodies, Monoclonal / Q000276:immunology; D015703:Antigens, CD / Q000032:analysis / Q000378:metabolism; D001158:Arteries / Q000166:cytology; D019002:CD56 Antigen / Q000032:analysis / Q000378:metabolism; D018959:CD57 Antigens / Q000032:analysis / Q000378:metabolism; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology; D004717:Endometrium / Q000098:blood supply / Q000737:chemistry / Q000166:cytology; D004730:Endothelium, Vascular / Q000166:cytology; D004847:Epithelial Cells / Q000166:cytology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D007633:Keratins / Q000032:analysis / Q000276:immunology; D007694:Killer Cells, Natural / Q000737:chemistry / Q000166:cytology; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins / Q000032:analysis / Q000378:metabolism; D009130:Muscle, Smooth / Q000166:cytology; D051920:NK Cell Lectin-Like Receptor Subfamily D; D019006:Neural Cell Adhesion Molecules / Q000032:analysis* / Q000235:genetics / Q000276:immunology; D010920:Placenta / Q000098:blood supply / Q000166:cytology*; D011247:Pregnancy; D011261:Pregnancy Trimester, First; D014327:Trophoblasts / Q000737:chemistry* / Q000166:cytology* / Q000378:metabolism; D014746:Vimentin / Q000032:analysis / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D019002:CD56 Antigen; D018959:CD57 Antigens; C497869:KLRD1 protein, human; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins; D051920:NK Cell Lectin-Like Receptor Subfamily D; D019006:Neural Cell Adhesion Molecules; D014746:Vimentin; D007633:Keratins