Qwarnström E E, Ostberg C O, Turk G L, Richardson C A, Bomsztyk K
Department of Pathology, University of Washington, Seattle 98195.
J Biol Chem. 1994 Dec 9;269(49):30765-8.
The nuclear factor kappa B, NF-kappa B, is activated by numerous inflammatory mediators, regulating biological responses that in part are dependent on the extracellular matrix. Analyses of the influence of cell-matrix interaction on NF-kappa B activation revealed that attachment to fibronectin caused an increase in NF-kappa B activity corresponding to 3-fold the level in cells plated on bare plastic. This effect was dependent on the degree of attachment and appeared to involve both the RGD motif of the cell-binding domain, and the heparin-binding domain of fibronectin. Fibronectin attachment specifically caused activation of the p50/p65 heterodimeric form of NF-kappa B, resulting in an increase of this complex to a level similar to that induced by cytokine stimulation. These data show that cell attachment has a pronounced influence on the level of NF-kappa B activity, affecting specific dimeric complexes, and suggest this to be a pathway through which effects depending on cell-matrix interaction can regulate cell behavior and cytokine responses.
核因子κB（NF-κB）可被多种炎症介质激活，调控部分依赖细胞外基质的生物学反应。对细胞-基质相互作用对NF-κB激活影响的分析表明，细胞黏附于纤连蛋白会导致NF-κB活性增加，相当于接种在裸塑料板上细胞水平的3倍。这种效应取决于黏附程度，似乎涉及细胞结合结构域的RGD基序以及纤连蛋白的肝素结合结构域。纤连蛋白黏附特异性地导致NF-κB的p50/p65异二聚体形式激活，使该复合物水平增加至与细胞因子刺激诱导的水平相似。这些数据表明细胞黏附对NF-κB活性水平有显著影响，影响特定的二聚体复合物，并提示这是一条依赖细胞-基质相互作用的效应可调节细胞行为和细胞因子反应的途径。
