Bertomeu M C, Gallo S, Lauri D, Haas T A, Orr F W, Bastida E, Buchanan M R
Department of Pathology, McMaster University, Hamilton, Ontario, Canada.
Clin Exp Metastasis. 1993 May;11(3):243-50. doi: 10.1007/BF00121167.
Previously, we have demonstrated that stimulation of endothelial cells (ECs) with interleukin-1 alpha (IL-1 alpha) enhances the synthesis and expression of the vitronectin receptor (VnR), promotes VnR-dependent adhesion of human A549 adenocarcinoma cells to ECs, and is associated with decreased EC 13-hydroxyoctadecadienoic acid (13-HODE) synthesis in vitro. To determine whether these observations are relevant in vivo, we examined the acute retention and subsequent metastasis of intravenously-injected B16F10 melanoma cells in murine lungs, in relation to vessel wall 13-HODE. In C57BL/6 mice pretreated with IL-1 alpha, vessel wall 13-HODE was decreased and B16F10 lung entrapment and metastasis were increased. The latter two events were blocked by pretreating the animals with the GRGDS peptide. These data suggest a relationship between vessel wall 13-HODE synthesis, adhesion molecule expression, and adhesion of B16F10 cells to the endothelium.
此前,我们已经证明,用白细胞介素-1α(IL-1α)刺激内皮细胞(ECs)可增强玻连蛋白受体(VnR)的合成和表达,促进人A549腺癌细胞依赖VnR黏附于ECs,并且在体外与ECs中13-羟基十八碳二烯酸(13-HODE)合成减少有关。为了确定这些观察结果在体内是否相关,我们研究了静脉注射的B16F10黑色素瘤细胞在小鼠肺中的急性滞留及随后的转移情况,以及与血管壁13-HODE的关系。在用IL-1α预处理的C57BL/6小鼠中,血管壁13-HODE减少,B16F10在肺中的滞留和转移增加。后两个事件可通过用GRGDS肽预处理动物来阻断。这些数据表明血管壁13-HODE合成、黏附分子表达以及B16F10细胞与内皮细胞黏附之间存在关联。