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

来源：

JOURNAL OF NEUROIMMUNOLOGY | 1997年 / 73卷 / 1-2期

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

页码：155 / 161

页数：7