Abstract：
The mammalian palate separates the oral and nasal cavities, facilitating proper feeding, respiration, and speech. Palatal shelves, composed of neural crest-derived mesenchyme and surrounding epithelium, are a pair of maxillary prominences contributing to this structure. Palatogenesis reaches completion upon the fusion of the midline epithelial seam (MES) following contact between medial edge epithelium (MEE) cells in the palatal shelves. This process entails numerous cellular and molecular occurrences, including apoptosis, cell proliferation, cell migration, and epithelial-mesenchymal transition (EMT). MicroRNAs (miRs) are small, endogenous, non-coding RNAs derived from double-stranded hairpin precursors that regulate gene expression by binding to target mRNA sequences. Although miR-200c is a positive regulator of E-cadherin, its role in palatogenesis remains unclear. This study aims to explore the role of miR-200c in palate development. Before contact with palatal shelves, mir-200c was expressed in the MEE along with E-cadherin. After palatal shelf contact, miR-200c was present in the palatal epithelial lining and epithelial islands surrounding the fusion region but absent in the mesenchyme. The function of miR-200c was investigated by utilizing a lentiviral vector to facilitate overexpression. Ectopic expression of miR-200c resulted in E-cadherin upregulation, impaired dissolution of the MES, and reduced cell migration for palatal fusion. The findings imply that miR-200c is essential in palatal fusion as it governs E-cadherin expression, cell death, and cell migration, acting as a non-coding RNA. This study may contribute to clarifying the underlying molecular mechanisms in palate formation and provides insights into potential gene therapies for cleft palate.
摘要：
哺乳动物的腭将口腔和鼻腔分开，促进适当的喂养，呼吸,和演讲。腭架,由神经c衍生的间充质和周围上皮组成，是一对上颌骨突出，有助于这种结构。在the架中的内侧边缘上皮（MEE）细胞之间接触后，中线上皮接缝（MES）融合后，腭形成就完成了。这个过程需要大量的细胞和分子发生，包括细胞凋亡,细胞增殖，细胞迁移，和上皮-间质转化（EMT）。microRNAs（miRs）很小，内源性,来自双链发夹前体的非编码RNA，通过与靶mRNA序列结合来调节基因表达。尽管miR-200c是E-cadherin的正调节因子,其在腭生中的作用尚不清楚.本研究旨在探讨miR-200c在腭发育中的作用。在接触腭架之前,mir-200c与E-钙粘蛋白一起在MEE中表达。腭架接触后，miR-200c存在于pal上皮衬里和融合区域周围的上皮岛中，但不存在于间充质中。通过利用慢病毒载体促进过表达来研究miR-200c的功能。miR-200c的异位表达导致E-cadherin上调，MES溶解受损，和减少细胞迁移的腭融合。研究结果表明，miR-200c在pal融合中是必不可少的，因为它控制着E-cadherin的表达，细胞死亡,和细胞迁移，作为非编码RNA。这项研究可能有助于阐明腭形成的潜在分子机制，并为腭裂的潜在基因治疗提供见解。
