Distribution of adhesion molecules on HeLa cells, platelets and endothelium in an in vitro model mimicking the early phase of metastasis. An immunogold electron microscopic study.
The aim of the present study was to obtain information about the distribution of various adhesion molecules within and on the surface of HeLa cells, platelets and endothelial cells in an in vitro model mimicking the early phase of metastasis. Suspensions of HeLa cells and human platelets, added to a medium of cultured human umbilical-vein endothelial cells, were stimulated by the addition of thrombin. Hirudin was added before thrombin in some experiments, and in other experiments the endothelium was pretreated with 0.5 mM acetylsalicylic acid (ASA). The distribution of platelet-endothelial cell adhesion molecule (PECAM), P-selectin, von Willebrand factor (vWf), fibrinogen (FG) and thrombospondin (TSP) was investigated on fixed material from the three experimental settings by using an immunogold electron-microscopic technique on frozen thin sections. Cells that had not been exposed to thrombin or any other type of stimulation were used as controls. PECAM was the only adhesion molecule detected on HeLa cells. It outlined the membrane on tumour cells that were not adherent to platelets in both basic and hirudin experiments. However, tumour cells in close proximity to activated platelets were unlabelled. In contrast, PECAM was detected on both platelets and endothelium in all experimental settings and in controls. P-selectin was only demonstrable on platelets in basic experiments. vWf was found both in endothelium and in platelets in controls and in all experimental settings. FG and TSP were found on platelets only, in a manner similar to that seen with vWf. Thus, among the adhesive factors examined in our experimental model, PECAM is the only one demonstrated on HeLa cells. This suggests that PECAM on tumour cells may play a role as adhesion molecule in the early stage of metastasis. P-selectin, vWf, FG and TSP were also consistently expressed. Therefore, these factors may contribute to the adhesive reactions involved in early metastasis.
Klementsen
B
B
Department of Morphology II, University of Tromsø, Norway.
Jørgensen
L
L
D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000378:metabolism*; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism*; D005340:Fibrinogen / Q000378:metabolism; D006367:HeLa Cells; D006801:Humans; D008562:Membrane Glycoproteins / Q000378:metabolism; D009362:Neoplasm Metastasis; D019007:P-Selectin / Q000378:metabolism; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D019699:Thrombospondins; D014841:von Willebrand Factor / Q000378:metabolism
D015815:Cell Adhesion Molecules; D008562:Membrane Glycoproteins; D019007:P-Selectin; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D019699:Thrombospondins; D014841:von Willebrand Factor; D005340:Fibrinogen; D001241:Aspirin