Michalides R, Volberg T, Geiger B
Department of Tumor Biology, The Netherlands Cancer Institute, Amsterdam.
Cell Adhes Commun. 1994 Dec;2(6):481-90. doi: 10.3109/15419069409014212.
Adherens-type junctions (AJ) are specialized intercellular contacts, mediated by cadherins and characterized by the association with actin filaments through a vinculin- and catenin-rich submembrane plaque. We describe here two mechanisms which potentiate AJ formation in mesenchymal cells. These include the augmentation of AJ by the co-expression of another adhesion molecule, namely NCAM, and the stimulation of tyrosine phosphorylation. These effects were obtained in NIH-3T3 cells, which, under normal conditions, have poor cadherin- and vinculin-containing intercellular junctions. The transfection of these cells with cDNA encoding the 140kD NCAM resulted in the extensive formation of cadherin- and vinculin-rich AJ, demonstrating a cooperativity between the two junctional systems. AJ could also be induced in 3T3, and in CEF and COS cells, upon a brief exposure to H2O2/vanadate, which elevates cellular levels of phosphotyrosine due to inhibition of tyrosine-specific phosphatases. This induction was, however, transient since prolonged exposure to H2O2/vanadate resulted in an overall destruction of AJ and detachment of cells from each other and from the extracellular matrix. AJ formation appears, therefore, to be modulated by a variety of factors including the level of expression of its intrinsic components, the cooperative effect of other adhesion molecules, and by tyrosine-phosphorylation.
黏附连接(AJ)是一种特殊的细胞间连接,由钙黏蛋白介导,其特征是通过富含纽蛋白和连环蛋白的亚膜斑块与肌动蛋白丝相连。我们在此描述了两种增强间充质细胞中AJ形成的机制。这些机制包括通过共表达另一种黏附分子(即神经细胞黏附分子,NCAM)来增强AJ,以及刺激酪氨酸磷酸化。这些效应在NIH-3T3细胞中得以实现,在正常条件下,这些细胞含有钙黏蛋白和纽蛋白的细胞间连接较差。用编码140kD NCAM的cDNA转染这些细胞,导致富含钙黏蛋白和纽蛋白的AJ广泛形成,证明了这两种连接系统之间的协同作用。短暂暴露于H2O2/钒酸盐后,3T3细胞、鸡胚成纤维细胞(CEF)和COS细胞中也可诱导AJ形成,由于酪氨酸特异性磷酸酶受到抑制,H2O2/钒酸盐会提高细胞内磷酸酪氨酸水平。然而,这种诱导是短暂的,因为长时间暴露于H2O2/钒酸盐会导致AJ整体破坏,细胞彼此以及与细胞外基质分离。因此,AJ的形成似乎受到多种因素的调节,包括其内在成分的表达水平、其他黏附分子的协同作用以及酪氨酸磷酸化。