NF-κB activation for constitutive expression of VCAM-1 and ICAM-1 on B lymphocytes and plasma cells

被引:69
作者
Xia, YF
Liu, LP
Zhong, CP
Geng, JG
机构
[1] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Shanghai 200031, Peoples R China
[2] Chinese Acad Sci, Shanghai Inst Biol Sci, Mol Cell Biol Lab, Shanghai 200031, Peoples R China
[3] Fudan Univ, Sch Med, Dept Histol & Embryol, Shanghai 200433, Peoples R China
[4] Tongji Univ, Sch Med, Dept Histol & Embryol, Shanghai 200092, Peoples R China
关键词
VCAM-1; ICAM-1; adhesion molecules; B-lymphocytes; plasma cells; NF-kappa B; transcriptional regulation;
D O I
10.1006/bbrc.2001.6067
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cytokine stimulation can activate NF-kappaB that triggers inducible expression of E-selectin, VCAM-1 (Vascular Cell Adhesion Molecule-1) and ICAM-1 (Intercellular Cell Adhesion Molecule-1) in endothelial cells. In the previous study, we have shown that B lymphocytes and plasma cells can express E-selectin by constitutive activation of NF-kappaB. Here we show that human B lymphocytes and ARH-77 plasma cells expressed VCAM-1 and ICAM-1 in a cytokine dispensable mechanism. NF-kappaB antagonists could inhibit their expressions in ARH-77 cells. The activities of NF-kappaB for VCAM-1 and ICAM-1 promoters prior to cytokine stimulation were detected in ARH-77 cells using electrophoretic mobility shift assays. Again, NF-kappaB antagonists could abrogate these promoter activities. Taken together, our results demonstrate that NF-kappaB activation is the underlying molecular mechanism for constitutive expression of E-selectin, VCAM-1, and ICAM-1 on human B lymphocytes and plasma cells. (C) 2001 Elsevier Science.
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页码:851 / 856
页数:6
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