Molecular Maternal Effect on Etiology of cleft lip nad palate in Fetal Mouse Model.

TGF-β 3介导的上皮间充质转化在正常的唇腭裂融合，但TGF-β 3如何在唇裂修复功能仍然是未知的。我们推测TGF-β 3通过增加间充质细胞的可用性促进胎儿唇裂修复和融合。在这项研究中，我们证明了小鼠胎儿唇裂可以通过胎儿手术修复，产生无瘢痕融合。在手术部位，我们首先观察到表达TGF-β 3的血小板输注，随后细胞周期蛋白D1和生腱蛋白C的表达增加，并伴有间充质细胞增殖增加。在体外无血清培养系统中，唇裂外植体在外源性TGF-β 3的存在下融合。培养的嘴唇也表现出上调细胞周期蛋白D1和tenascin-C的表达。这些研究结果表明，显微手术修复胎儿唇裂，产生无瘢痕融合介导的TGF-β 3调节间充质细胞的增殖和迁移的网站的修复。

TGF-b3 mediates epithelial-mesenchymal transformation during normal fusion of lip and palate, but how TGF-b3 functions during cleft lip repair remains unexplored. We hypothesize that TGF-b3 promotes fetal cleft lip repair and fusion by increasing the availability of nesenchymal cells. In this investigation, we demonstrated that cleft lips in mouse fetuses were repaired by fetal surgery, producing scarless fusion. At the site of the operation, we first observed an infusion of platelet expressing TGF-b3, followed by increased expression of cyclin D1 and tenascin-C, and coupled with increased mesenchymal cell proliferation. In an ex vivo serumless culture system, cleft lip explants fused in the presence of exogenous TGF-b3. Cultured lips also showed up-regulation in cyclin D1 and tenascin-C expression. These findings suggest that microsurgical repair of cleft lip in the fetus that produced scarless fusion is mediated by TGF-b3 regulation of mesenchymal cell proliferation and migration at the site of repair.