Tumor cell-platelet-endothelial cell interactions and prostaglandin metabolism.
We have proposed that tumor cell induction of platelet aggregation facilitates tumor cell attachment to endothelium and that this attachment is limited by endogenous PGI2. We have developed an in vitro model to study tumor cell-platelet-endothelial cell interactions in which endothelial cells are grown on microcarrier beads. Untreated endothelial cells inhibit tumor cell-induced platelet aggregation, as well as tumor cell attachment to endothelial cells. Inhibition of endothelial cell PGI2 production by indomethacin obviates this inhibition.
D000818:Animals; D002279:Carcinoma 256, Walker / Q000473:pathology / Q000503:physiopathology*; D002448:Cell Adhesion; D002450:Cell Communication; D002478:Cells, Cultured; D004727:Endothelium / Q000473:pathology / Q000503:physiopathology*; D011464:Epoprostenol / Q000378:metabolism*; D010974:Platelet Aggregation; D051381:Rats
D011464:Epoprostenol