Klementsen B, Jørgensen L
Department of Morphology II, University of Tromsø, Norway.
APMIS. 1997 May;105(5):391-401. doi: 10.1111/j.1699-0463.1997.tb00586.x.
The aim of the study was to obtain more information about the mechanisms involved in the initial adhesion of tumour cells to endothelial cell during metastasis. In a previous paper, we found that addition of both platelets and thrombin increased the adhesion of tumour cells to cultured endothelial cells within 15 min, compared to when either one or both of the ingredients were absent. In the present study, HeLa cells, prelabelled with radioactive 51Cr, human platelets, and thrombin, were added to the medium in dishes of endothelial cells. The dishes were then shaken for 15 min at 37 degrees C. Scanning and transmission electron micrographs showed HeLa cells adhering to the endothelium either together with platelets or without them. In other experiments, the endothelium was pretreated for 30 min with either of the following: 0.5 mM or 0.1 mM acetylsalicylic acid (ASA); 0.5 mM or 0.1 mM Na-salicylate (NaS). Pretreatment of the endothelium with 0.5 mM ASA significantly increased the percentage of adherent tumour cells, while 0.1 mM ASA and the two concentrations of NaS caused only minor changes. In addition, the ASA-treatment caused more HeLa cells to adhere without platelets while NaS-treatment caused more HeLa cells to adhere together with platelets. Release of 51Cr from HeLa cells during the experimental period was also measured; the addition of thrombin and platelets did not change the 51Cr release significantly. In separate experiments, HeLa cells and platelets were mixed without the presence of endothelial cells. Transmission electron micrographs showed that in the absence of thrombin, mixed HeLa cells and platelets did not react with each other; when thrombin was added they formed co-aggregates. In conclusion, we show that in our experimental model HeLa cells adhere to the endothelium in two ways, both with and without platelets. The production of prostacyclin in the endothelial cells has an inhibitory effect on tumour cell adhesion. Without thrombin, the HeLa cells are not capable of activating platelets.
本研究的目的是获取更多关于肿瘤细胞在转移过程中与内皮细胞初始黏附所涉及机制的信息。在之前的一篇论文中,我们发现与单独缺少血小板或凝血酶,或两者都缺少时相比,同时添加血小板和凝血酶可在15分钟内增加肿瘤细胞与培养的内皮细胞的黏附。在本研究中,将预先用放射性51Cr标记的HeLa细胞、人血小板和凝血酶添加到内皮细胞培养皿的培养基中。然后将培养皿在37℃下振荡15分钟。扫描电子显微镜和透射电子显微镜图像显示,HeLa细胞与血小板一起或不与血小板一起黏附在内皮上。在其他实验中,用以下任何一种物质对内皮进行30分钟预处理:0.5 mM或0.1 mM乙酰水杨酸(ASA);0.5 mM或0.1 mM水杨酸钠(NaS)。用0.5 mM ASA预处理内皮可显著增加黏附肿瘤细胞的百分比,而0.1 mM ASA和两种浓度的NaS仅引起微小变化。此外,ASA处理导致更多HeLa细胞在无血小板的情况下黏附,而NaS处理导致更多HeLa细胞与血小板一起黏附。还测量了实验期间HeLa细胞中51Cr的释放;添加凝血酶和血小板并未显著改变51Cr的释放。在单独的实验中,将HeLa细胞和血小板在无内皮细胞的情况下混合。透射电子显微镜图像显示,在无凝血酶的情况下,混合的HeLa细胞和血小板彼此不发生反应;添加凝血酶后它们形成共聚集物。总之,我们表明在我们的实验模型中,HeLa细胞以两种方式黏附在内皮上,有血小板和无血小板。内皮细胞中前列环素的产生对肿瘤细胞黏附有抑制作用。没有凝血酶,HeLa细胞无法激活血小板。