Matsuda Miho, Kubo Akiharu, Furuse Mikio, Tsukita Shoichiro
Department of Cell Biology, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.
J Cell Sci. 2004 Mar 1;117(Pt 7):1247-57. doi: 10.1242/jcs.00972.
Tight junctions (TJs) seal the intercellular space of epithelial cells, while individual epithelial cells move against adjacent cells in cellular sheets. To observe TJs in live epithelial cellular sheets, green fluorescent protein (GFP) was fused to the N-terminus of claudin-3 (a major cell adhesion molecule of TJs), which was stably expressed at a level that was approximately 50% of that of endogenous claudin-3 in mouse Eph4 epithelial cells. Under confluent culture conditions, individual cells moved within cellular sheets, which was associated with the remodeling of TJs. However, during this remodeling, GFP-positive TJs did not lose their structural continuity. When TJs between two adjacent cells decreased in length during this remodeling, GFP-claudin-3 was frequently pinched off as a granular structure from GFP-positive TJs together with endogenous claudins. Co-culture experiments, as well as electron microscopy, revealed that the two apposed membranes of TJs were not detached, but co-endocytosed into one of the adjacent cells. Interestingly, other TJ components such as occludin, JAM and ZO-1 appeared to be dissociated from claudins before this endocytosis. The endocytosis of claudins was facilitated when the intercellular motility was upregulated by wounding the cellular sheets. These findings suggest that this peculiar internalization of claudins plays a crucial role in the remodeling of TJs, and that the fine regulation of this endocytosis is important for TJs to seal the intercellular space of epithelial cells that are moving against adjacent cells within cellular sheets.
紧密连接(TJs)封闭上皮细胞的细胞间隙,而单个上皮细胞在细胞层中与相邻细胞相对移动。为了在活的上皮细胞层中观察紧密连接,绿色荧光蛋白(GFP)与claudin-3(紧密连接的一种主要细胞粘附分子)的N端融合,claudin-3在小鼠Eph4上皮细胞中的稳定表达水平约为内源性claudin-3的50%。在汇合培养条件下,单个细胞在细胞层内移动,这与紧密连接的重塑有关。然而,在这种重塑过程中,GFP阳性的紧密连接并没有失去其结构连续性。当两个相邻细胞之间的紧密连接在重塑过程中长度减小时,GFP-claudin-3经常作为颗粒结构与内源性claudin一起从GFP阳性的紧密连接中被夹断。共培养实验以及电子显微镜显示,紧密连接的两个相对膜并未分离,而是共同内吞进入相邻细胞之一。有趣的是,在这种内吞作用之前,其他紧密连接成分如闭合蛋白、连接粘附分子(JAM)和紧密连接蛋白1(ZO-1)似乎已与claudin分离。当通过损伤细胞层上调细胞间运动性时,claudin的内吞作用得到促进。这些发现表明,claudin的这种特殊内化在紧密连接的重塑中起关键作用,并且这种内吞作用的精细调节对于紧密连接封闭上皮细胞在细胞层中与相邻细胞相对移动时的细胞间隙很重要。