Macaque intra-arterial trophoblast and extravillous trophoblast of the cell columns and cytotrophoblastic shell express neural cell adhesion molecule (NCAM)

Abstract

Background: During placental development in higher primates trophoblast cells originating in the cell columns migrate along endometrial surfaces to form the cytotrophoblastic shell. A subpopulation of these cells invades uterine arteries, where they migrate on the surface of endothelium, against the flow of blood. These intra-arterial cells become sequestered in the walls of the arteries where they are referred to as intramural trophoblast. Because migration depends upon binding the cell surface to other cells or to extracellular matrix, we investigated the potential role of neural cell adhesion molecule (NCAM, CD56) in arterial invasion by trophoblast cells.

Methods: Tissues from macaque placentas and endometrium were fixed and embedded in paraffin. Standard immunoperoxidase methods were used to identify NCAM.

Results: NCAM labeled cells were present within spiral arteries of the decidua basalis. Trophoblast cells within or adjacent to the arterial lumen were distinctly NCAM positive, whereas most intramural trophoblast cells revealed reduced or no reactivity for NCAM. Maternal endothelial cells and villous trophoblast cells were negative. Uterine veins were tapped by trophoblast but did not contain migratory cells. The cell columns of early pregnancy contained cells outlined by rims of reactivity for NCAM. Labeled cells were also seen in the cytotrophoblastic shell, arranged as discontinuous groups. These groups variably occupied the entire thickness of the shell, or only the proximal (adjacent to the intervillous space) or distal layers of the shell. Later in gestation, the cytotrophoblastic shell developed a different pattern of staining, such that only cells located nearer to the intervillous space or near the tips of the anchoring villi were positive.

Conclusions: We conclude that NCAM is one of a group of cell adhesion molecules that participates in trophoblast cell adhesion during migration within maternal arteries. NCAM appears to be active in trophoblast-trophoblast cell interactions. It may also contribute to binding trophoblast cells to the surfaces of arterial endothelium as well as extracellular matrix molecules of the arterial wall. After secondary invasion into the arterial walls NCAM is down-regulated, possibly in response to the appearance of extracellular matrix capsules, where other cell adhesion molecules may appear.