Sun D, Mcalmon K R, Davies J A, Bernfield M, Hay E D
Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Int J Dev Biol. 1998 Jul;42(5):733-6.
Epithelial-mesenchymal transformation (EMT) is the key mechanism for fusion and confluence of the rodent palate. During this process, medial edge epithelia (MEE) form a midline seam that subsequently transforms to mesenchymal cells. We studied syndecan-1 and E-cadherin, two molecules which have been shown to promote the epithelial phenotype, to determine their fate during palatal EMT. We found that both syndecan-1 and E-cadherin are expressed on basolateral surfaces of the MEE at day 14. Twelve hours later, when a midline seam has formed, syndecan-1 and E-cadherin are still present on its basal and lateral epithelial surfaces and they persist after the seam breaks up into epithelial islands. Then, expression of both molecules is lost simultaneously and abruptly when EMT occurs. On the contrary, previous in vitro studies of cell lines transfected with antisense cDNAs suggested that loss of syndecan-1 would lead to loss of E-cadherin or vice versa. We conclude that in vivo, synthesis of both E-cadherin and syndecan-1 is downregulated synchronously by the initiation of EMT, leading to an effective and correctly timed conversion of the epithelial cells to mesenchyme.
上皮-间质转化（EMT）是啮齿动物腭部融合与汇合的关键机制。在此过程中，内侧边缘上皮（MEE）形成一条中线缝，随后该中线缝转变为间充质细胞。我们研究了syndecan-1和E-钙黏蛋白这两种已被证明可促进上皮表型的分子，以确定它们在腭部EMT过程中的命运。我们发现，在第14天时，syndecan-1和E-钙黏蛋白均在MEE的基底外侧表面表达。12小时后，当中线缝形成时，syndecan-1和E-钙黏蛋白仍存在于其基底和外侧上皮表面，并且在缝线分裂成上皮岛后它们依然存在。然后，当EMT发生时，这两种分子的表达同时且突然丧失。相反，先前对用反义cDNA转染的细胞系进行的体外研究表明，syndecan-1的缺失会导致E-钙黏蛋白的缺失，反之亦然。我们得出结论，在体内，EMT的启动会同步下调E-钙黏蛋白和syndecan-1的合成，从而导致上皮细胞有效且适时地转化为间充质。
