Endothelial leukocyte adhesion molecule-1-dependent adhesion of colon carcinoma cells to vascular endothelium is inhibited by an antibody to Lewis fucosylated type I carbohydrate chain.

Endothelial leukocyte adhesion molecule-1-dependent adhesion of colon carcinoma cells to vascular endothelium is inhibited by an antibody to Lewis fucosylated type I carbohydrate chain.
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Lewis 岩藻糖基化 I 型糖链抗体可抑制结肠癌细胞与血管内皮的内皮白细胞粘附分子 1 依赖性粘附。

DOI:
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发表时间:
1992
期刊:
Laboratory investigation; a journal of technical methods and pathology
影响因子:
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通讯作者:
Sylvie Ménard
Sylvie Ménard
中科院分区:
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文献类型:
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作者:
Elisabetta Dejana;I. Martìn‐padura;D. Lauri;S. Bernasconi;M. Bani;A. Garofalo;R. Giavazzi;J. Magnani;A. Mantovani;Sylvie Ménard

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内皮白细胞黏附分子 - 1(ELAM - 1)已被确定为结肠癌细胞与白细胞介素 - 1(IL - 1)激活的内皮细胞黏附的介质。为了鉴定结肠癌细胞中的ELAM - 1配体,我们筛选了一系列针对这些细胞的11种单克隆抗体,发现只有一种MBr8能够抑制IL - 1诱导的HT29和SW948结肠癌细胞系与内皮细胞黏附的增加。相比之下,MBr8不与多形核细胞、单核细胞和淋巴细胞结合,也不抑制多形核细胞与IL - 1激活的内皮细胞的黏附。正如预期的那样,一种ELAM - 1单克隆抗体强烈抑制IL - 1诱导的HT29、SW948和多形核细胞黏附的增加。作为阴性对照,使用了MG63骨肉瘤细胞。这些细胞更有效地黏附于IL - 1激活的内皮细胞,但MBr8和ELAM - 1单克隆抗体不影响它们的黏附。还在体内实验系统中测试了MBr8的作用。如先前所述,在给予IL - 1的裸鼠中,放射性标记的HT29细胞在肺中的滞留增加。给裸鼠施用MBr8或用其预处理肿瘤细胞抑制了这种效应。这些数据表明,细胞与ELAM - 1的黏附可能由不同的、细胞类型特异性的糖配体介导。
Endothelial leukocyte adhesion molecule-1 (ELAM-1) has been determined to be the mediator of adhesion of colon carcinoma cells to interleukin-1 (IL-1)-activated endothelial cells. To identify ELAM-1 ligand in colon carcinoma cells, we have screened a series of 11 monoclonal antibodies directed to these cells and found that only one MBr8 was able to inhibit the IL-1-induced increment in adhesion of HT29 and of SW948 colon carcinoma lines to endothelial cells. In contrast, MBr8 did not bind to polymorphonuclear cells, monocytes, and lymphocytes and did not inhibit polymorphonuclear adhesion to IL-1-activated endothelial cells. As expected, an ELAM-1 monoclonal antibody strongly inhibited IL-1 induced increment of adhesion of HT29, SW948, and polymorphonuclear cells. As negative control, MG63 osteosarcoma cells were used. These cells adhere more efficiently to IL-1 activated endothelial cells but MBr8 and ELAM-1 monoclonal antibodies did not affect their adhesion. The effect of MBr8 was also tested in an experimental system in vivo. As described previously, radiolabeled HT29 cell retention in the lung of nude mice was increased in animals given IL-1. MBr8 administration to nude mice or pretreatment of tumor cells with it inhibited this effect. These data suggest that cell adhesion to ELAM-1 might be mediated by different, cell type specific, sugar ligands.