Roos E, Tulp A, Middelkoop O P, van de Pavert I V
J Natl Cancer Inst. 1984 May;72(5):1173-80.
Interactions were studied between highly metastatic murine MB6A lymphosarcoma cells and rat liver endothelial cells that had been isolated by collagenase perfusion and purified by unit gravity sedimentation. Experiments were performed on the day of isolation. MB6A cells were observed to adhere to the endothelial cells. Addition of rat serum had a striking effect: The endothelial cells spread over the MB6A cell surface, engulfing the tumor cells. The factor involved was nondialyzable and also was present in rat plasma. Similar interactions were seen with highly metastatic ESb and MDAY-D2 lymphoma cells and with nonmetastatic Eb cells. Low-metastatic GRSL 34 leukemia and TA3/Ha ascites mammary carcinoma cells did not adhere to the endothelial cells. With this in vitro model the molecular mechanisms of adhesion to liver endothelium were studied. As a first step, univalent antibodies against MB6A cells were found to inhibit adhesion, indicating involvement of specific cell surface molecules.
研究了高转移性小鼠MB6A淋巴肉瘤细胞与通过胶原酶灌注分离并用单位重力沉降法纯化的大鼠肝内皮细胞之间的相互作用。在分离当天进行实验。观察到MB6A细胞粘附于内皮细胞。添加大鼠血清有显著效果:内皮细胞铺展在MB6A细胞表面,吞噬肿瘤细胞。所涉及的因子不能透析,且也存在于大鼠血浆中。在高转移性ESb和MDAY-D2淋巴瘤细胞以及非转移性Eb细胞中也观察到类似的相互作用。低转移性GRSL 34白血病细胞和TA3/Ha腹水乳腺癌细胞不粘附于内皮细胞。利用这个体外模型研究了与肝内皮细胞粘附的分子机制。第一步,发现针对MB6A细胞的单价抗体可抑制粘附,表明特定细胞表面分子参与其中。