Xia Y F, Liu L P, Zhong C P, Geng J G
Laboratory of Molecular Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Biochem Biophys Res Commun. 2001 Dec 14;289(4):851-6. doi: 10.1006/bbrc.2001.6067.
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.
细胞因子刺激可激活核因子-κB，从而触发内皮细胞中E-选择素、血管细胞黏附分子-1（VCAM-1）和细胞间黏附分子-1（ICAM-1）的诱导性表达。在先前的研究中，我们已表明B淋巴细胞和浆细胞可通过核因子-κB的组成性激活来表达E-选择素。在此我们表明，人B淋巴细胞和ARH-77浆细胞以一种不依赖细胞因子的机制表达VCAM-1和ICAM-1。核因子-κB拮抗剂可抑制它们在ARH-77细胞中的表达。使用电泳迁移率变动分析在ARH-77细胞中检测了细胞因子刺激前核因子-κB对VCAM-1和ICAM-1启动子的活性。同样，核因子-κB拮抗剂可消除这些启动子活性。综上所述，我们的结果表明核因子-κB激活是E-选择素、VCAM-1和ICAM-1在人B淋巴细胞和浆细胞上组成性表达的潜在分子机制。
