5 TUMOR NECROSIS FACTOR-INDUCIBLE CELL-ADHESION MECHANISMS ON THE SURFACE OF MOUSE ENDOTHELIOMA CELLS MEDIATE THE BINDING OF LEUKOCYTES
5 TUMOR NECROSIS FACTOR-INDUCIBLE CELL-ADHESION MECHANISMS ON THE SURFACE OF MOUSE ENDOTHELIOMA CELLS MEDIATE THE BINDING OF LEUKOCYTES
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DOI：
10.1083/jcb.121.3.655
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发表时间：
1993-05-01
影响因子：
7.8
通讯作者：
VESTWEBER, D
中科院分区：
文献类型：
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作者：
HAHNE, M;JAGER, U;VESTWEBER, D
我们区分了五种由肿瘤坏死因子-α诱导的细胞在小鼠微血管内皮细胞上的黏附机制，它们介导了不同类型的白细胞的结合。这些机制中的三个可以被鉴定为ICAM-1、VCAM-1和E-选择素的小鼠同源物，后者由新的mAb21KC10定义。第四种肿瘤坏死因子-α诱导的细胞黏附机制被针对小鼠P-选择素的抗体阻断。我们最近发现，肿瘤坏死因子-α刺激小鼠内皮瘤细胞合成P-选择素(A.Weller，S.Isenmann，D.Vestweber)。1992年。J.Biol.化学。267：15176-15183)。在这里，我们发现，这种刺激导致细胞表面在刺激后4小时内达到最高水平，而同样的内皮瘤细胞也能够在PMA刺激后几分钟内上调细胞表面的P-选择素。这两种作用都是相加的。第五种肿瘤坏死因子诱导的细胞黏附机制是通过介导与小鼠单核/巨噬细胞系J774的结合来确定的。这种黏附机制不会被针对任何其他TURE凸轮的抗体抑制；它在7度C下工作良好(与ICAM-1和VCAM-1相反)，在肿瘤坏死因子诱导16小时后与4小时后一样活跃(与E-和P-选择素相反)。此外，尽管ICAM-1、VCAM-1、E-选择素和P-选择素在三种内皮瘤细胞系上都能很好地发挥作用，但这种新的黏附机制只在三种内皮瘤细胞系中的两种上发挥作用，在第三种上皮细胞系上检测不到。因此，除了已知的三种已知的肿瘤坏死因子诱导的细胞间黏附分子，ICAM-1。VCAM-1和E-选择素，以及P-选择素和第五种，分子上尚不清楚的细胞黏附机制，是在小鼠内皮瘤细胞表面诱导的肿瘤坏死因子。
We have distinguished five TNF-alpha-inducible cell adhesion mechanisms on microvasculature-derived endothelioma cells of the mouse which mediate the binding of different types of leukocytes. Three of these mechanisms could be identified as the mouse homologs of ICAM-1, VCAM-1, and E-selectin, of which the latter was defined by the novel mAb 21KC10. The fourth TNF-alpha-inducible cell adhesion mechanism was blocked by antibodies specific for mouse P-selectin. We have recently shown that TNF-alpha stimulates the synthesis of P-selectin in mouse endothelioma cells (A. Weller, S. Isenmann, D. Vestweber. 1992. J. Biol. Chem. 267:15176-15183). Here we show that this stimulation leads to maximal cell surface expression levels within 4 h after stimulation while the same endothelioma cells are also able to upregulate P-selectin at the cell surface within minutes after stimulation with PMA. Both effects are additive.The fifth TNF-induced cell adhesion mechanism is defined by mediating the binding to the mouse monocyte/macrophage cell line J774. This adhesion mechanism is not inhibited by antibodies against any of the other tour CAMs; it functions well at 7-degrees-C (in contrast to ICAM-1 and VCAM-1) and it is as active after 16 h of TNF induction as after 4 h (in contrast to E- and P-selectin). Furthermore, this new adhesion mechanism only functions on two of three endothelioma cell lines and is undetectable on the third, although ICAM-1, VCAM-1, E-selectin, and P-selectin could be demonstrated to function well on this cell line. Thus, in addition to the three known TNF-inducible CAMs, ICAM-1. VCAM-1, and E-selectin, also P-selectin and a fifth, as yet molecularly undefined cell adhesion mechanism, are TNF inducible at the cell surface of mouse endothelioma cells.