Vainio S, Jalkanen M, Thesleff I
Department of Pedodontics and Orthodontics, University of Helsinki, Finland.
J Cell Biol. 1989 May;108(5):1945-53. doi: 10.1083/jcb.108.5.1945.
Morphogenesis of embryonic organs is regulated by epithelial-mesenchymal interactions associating with changes in the extracellular matrix (ECM). The response of the cells to the changes in the ECM must involve integral cell surface molecules that recognize their matrix ligand and initiate transmission of signal intracellularly. We have studied the expression of the cell surface proteoglycan, syndecan, which is a matrix receptor for epithelial cells (Saunders, S., M. Jalkanen, S. O'Farrell, and M. Bernfield. J. Cell Biol. In press.), and the matrix glycoprotein, tenascin, which has been proposed to be involved in epithelial-mesenchymal interactions (Chiquet-Ehrismann, R., E. J. Mackie, C. A. Pearson, and T. Sakakura. 1986. Cell. 47:131-139) in experimental tissue recombinations of dental epithelium and mesenchyme. Our earlier studies have shown that in mouse embryos both syndecan and tenascin are intensely expressed in the condensing dental mesenchyme surrounding the epithelial bud (Thesleff, I., M. Jalkanen, S. Vainio, and M. Bernfield. 1988. Dev. Biol. 129:565-572; Thesleff, I., E. Mackie, S. Vainio, and R. Chiquet-Ehrismann. 1987. Development. 101:289-296). Analysis of rat-mouse tissue recombinants by a monoclonal antibody against the murine syndecan showed that the presumptive dental epithelium induces the expression of syndecan in the underlying mesenchyme. The expression of tenascin was induced in the dental mesenchyme in the same area as syndecan. The syndecan and tenascin positive areas increased with time of epithelial-mesenchymal contact. Other ECM molecules, laminin, type III collagen, and fibronectin, did not show a staining pattern similar to that of syndecan and tenascin. Oral epithelium from older embryos had lost its ability to induce syndecan expression but the presumptive dental epithelium induced syndecan expression even in oral mesenchyme of older embryos. Our results indicate that the expression of syndecan and tenascin in the tooth mesenchyme is regulated by epithelial-mesenchymal interactions. Because of their early appearance, syndecan and tenascin may be used to study the molecular regulation of this interaction. The similar distribution patterns of syndecan and tenascin in vivo and in vitro and their early appearance as a result of epithelial-mesenchymal interaction suggest that these molecules may be involved in the condensation and differentiation of dental mesenchymal cells.
胚胎器官的形态发生受上皮-间充质相互作用调控,这种相互作用与细胞外基质(ECM)的变化相关。细胞对ECM变化的反应必定涉及完整的细胞表面分子,这些分子识别其基质配体并启动细胞内信号传递。我们研究了细胞表面蛋白聚糖syndecan的表达,它是上皮细胞的一种基质受体(桑德斯,S.,M. 贾尔卡宁,S. 奥法雷尔,和M. 伯恩菲尔德。《细胞生物学杂志》即将发表),以及基质糖蛋白腱生蛋白,有人提出它参与上皮-间充质相互作用(奇凯特-埃里斯曼,R.,E. J. 麦基,C. A. 皮尔逊,和T. 坂仓。1986年。《细胞》。47:131 - 139),在牙上皮和间充质的实验性组织重组中进行了研究。我们早期的研究表明,在小鼠胚胎中,syndecan和腱生蛋白在围绕上皮芽的凝聚牙间充质中强烈表达(特斯莱夫,I.,M. 贾尔卡宁,S. 瓦尼奥,和M. 伯恩菲尔德。1988年。《发育生物学》。129:565 - 572;特斯莱夫,I.,E. 麦基,S. 瓦尼奥,和R. 奇凯特-埃里斯曼。1987年。《发育》。101:289 - 296)。用抗小鼠syndecan的单克隆抗体分析大鼠-小鼠组织重组体表明,假定的牙上皮诱导其下方间充质中syndecan的表达。腱生蛋白的表达在与syndecan相同的区域的牙间充质中被诱导。syndecan和腱生蛋白阳性区域随着上皮-间充质接触时间的增加而增加。其他ECM分子,层粘连蛋白、III型胶原蛋白和纤连蛋白,没有显示出与syndecan和腱生蛋白相似的染色模式。来自较老胚胎的口腔上皮失去了诱导syndecan表达的能力,但假定的牙上皮即使在较老胚胎的口腔间充质中也能诱导syndecan表达。我们的结果表明,牙间充质中syndecan和腱生蛋白的表达受上皮-间充质相互作用调控。由于它们出现得早,syndecan和腱生蛋白可用于研究这种相互作用的分子调控。syndecan和腱生蛋白在体内和体外相似的分布模式以及它们由于上皮-间充质相互作用而早期出现,表明这些分子可能参与牙间充质细胞的凝聚和分化。