TGF-B2 and soluble p55 TNFR modulate VCAM-1 expression in glioma cells and brain derived endothelial cells

被引:13
作者
Chen, TC
Hinton, DR
Yong, VW
Hofman, FM
机构
[1] UNIV SO CALIF,SCH MED,DEPT PATHOL,LOS ANGELES,CA 90033
[2] UNIV SO CALIF,SCH MED,DEPT NEUROSURG,LOS ANGELES,CA 90033
[3] MCGILL UNIV,MONTREAL NEUROL HOSP & INST,DEPT NEUROL & NEUROSURG,MONTREAL,PQ,CANADA
关键词
brain microvessel endothelium; soluble TNFR; VCAM-1; TGF-B2; gliomas;
D O I
10.1016/S0165-5728(96)00190-7
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Transforming growth factor beta-2 (TGF-B2) is secreted by glioma cells and is known to decrease leukocyte-endothelium interaction. TGF-B2 alone and in conjunction with soluble tumor necrosis factor (TNF) p55 receptor, was found to decrease the expression of TNF induced VCAM-1 on the malignant glioma cell line A-172 and human cerebral microvessel endothelial (CNS-EC) cells. Co-culture of A-172 glioma cells led to a decrease in VCAM-1 expression; this effect on CNS-EC in co-culture could be simulated by glioma supernatant alone. These results suggest that malignant gliomas, by secreting TGF-B2 and releasing soluble TNF receptors, modulate adhesion molecules.
引用
收藏
页码:155 / 161
页数:7
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