Expression of platelet-endothelial cell adhesion molecule-1 (PECAM) by macaque trophoblast cells during invasion of the spiral arteries

✍ Scribed by Blankenship, Thomas N. ;Enders, Allen C.

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 965 KB
• Volume: 247
• Category: Article
• ISSN: 0003-276X
• DOI: 10.1002/(sici)1097-0185(199703)247:3<413::aid-ar13>3.0.co;2-s

✦ Synopsis

Background: Placental development in higher primates is characterized by the invasion of uterine blood vessels by trophoblast cells. These cells proceed to migrate within uterine spiral arteries, opposite to the direction of normal blood flow. Observations indicate adhesion of intra-arterial trophoblast to endothelium as well as to adjacent trophoblast cells. Methods: Macaque placenta and endometrial tissues were collected from day 15 of pregnancy (implantation begins on day 9) to term. Standard indirect immunoperoxidase methods were used to identify plateletendothelial cell adhesion molecule-1 (PECAM), cytokeratins, and factor VIII-related antigen.

Results: In early specimens arterioles were often nearly occluded by cytokeratin-labeled trophoblast cells. Adjacent sections revealed the presence of PECAM on these trophoblast cells and on the endothelium. After day 30 the invaded arteries usually contained a re-formed lumen, and trophoblast cells were increasingly evident in the modified walls of arteries, where PECAM labeling was often reduced on cells distant from the lumen. Endothelium of both invaded and uninvaded uterine vessels retained PECAM reactivity throughout gestation. Trophoblast cells of the cell columns, cytotrophoblastic shell, and mid-to late-gestation chorionic plate were also reactive for PECAM. Villous cytotrophoblast cells did not express PECAM, but a dense border of PECAM was consistently present on the apical surfaces of syncytial trophoblast.

Conclusions: Because PECAM functions as a counter-ligand for PECAM via homophilic binding, we conclude that this molecule is directly involved in adhesion of trophoblast cells to arterial endothelium in addition to maintaining cohesion between some subpopulations of cytotrophoblast cells.