Regulation of the epithelial adhesion molecule CEACAM1 is important for palate formation.
Regulation of the epithelial adhesion molecule CEACAM1 is important for palate formation.
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DOI：
10.1371/journal.pone.0061653
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Sakai T
中科院分区：
文献类型：
--
作者：
Mima J;Koshino A;Oka K;Uchida H;Hieda Y;Nohara K;Kogo M;Chai Y;Sakai T
腭裂是遗传和环境因素共同作用的结果，发生在双侧腭架不能融合的时候。本研究的目的是寻找与小鼠腭形成有关的新基因。应用GeneChip®微阵列技术分析了腭融合前、融合中和融合后不同发育阶段小鼠胚胎腭组织的基因表达。Ceacam1是上颚形成过程中高度上调的基因之一，并通过实时荧光定量PCR证实了这一点。免疫组化染色显示CEACAM1存在于融合前腭上皮中，并在融合过程中降解。为了研究CEACAM1的发育作用，我们在胚胎小鼠上颚器官培养中添加了功能阻断抗体。该功能阻断抗体抑制腭融合。为了研究CEACAM1的后续发育作用，我们对CEACAM1缺陷（CEACAM1−/−）小鼠进行了表征。即使在E16.0天，Ceacam1 - / -小鼠胚胎腭中线的上皮细胞也存在异常，并且腭融合延迟。Ceacam1−/−小鼠腭上皮tgf - β3的表达、细胞凋亡和细胞增殖未受影响。然而，CEACAM1在tgf β缺乏小鼠的剩余MEE中保留了表达。这些结果表明CEACAM1通过上皮细胞粘附参与腭融合的启动。
Cleft palate results from a mixture of genetic and environmental factors and occurs when the bilateral palatal shelves fail to fuse. The objective of this study was to search for new genes involved in mouse palate formation. Gene expression of murine embryonic palatal tissue was analyzed at various developmental stages before, during, and after palate fusion using GeneChip® microarrays. Ceacam1 was one of the highly up-regulated genes during palate formation, and this was confirmed by quantitative real-time PCR. Immunohistochemical staining showed that CEACAM1 was present in prefusion palatal epithelium and was degraded during fusion. To investigate the developmental role of CEACAM1, function-blocking antibody was added to embryonic mouse palate in organ culture. Palatal fusion was inhibited by this function-blocking antibody. To investigate the subsequent developmental role of CEACAM1, we characterized Ceacam1-deficient (Ceacam1 −/−) mice. Epithelial cells persisted abnormally at the midline of the embryonic palate even on day E16.0, and palatal fusion was delayed in Ceacam1 −/− mice. TGFβ3 expression, apoptosis, and cell proliferation in palatal epithelium were not affected in the palate of Ceacam1−/−mice. However, CEACAM1 expression was retained in the remaining MEE of TGFβ-deficient mice. These results suggest that CEACAM1 has roles in the initiation of palatal fusion via epithelial cell adhesion.
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