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首页> 外文期刊>The international journal of developmental biology >Amniotic fluid induces rapid epithelialization in the experimentally ruptured fetal mouse palate - implications for fetal wound healing
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Amniotic fluid induces rapid epithelialization in the experimentally ruptured fetal mouse palate - implications for fetal wound healing

机译：羊水在实验性破裂的胎儿小鼠上颚中迅速上皮化-对胎儿伤口愈合有影响

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摘要

Cleft of the secondary palate is one of the most common congenital birth defects in humans. The primary cause of cleft palate formation is a failure of fusion of bilateral palatal shelves, but rupture of the once fused palate has also been suggested to take place in utero. The possibility of post-fusion rupture of the palate in humans has hardly been accepted, mainly because in all the cleft palate cases, the cleft palatal edge is always covered with intact epithelium. To verify whether the intrauterine environment of the fetus plays roles in wound healing when the once fused palate is torn apart, we artificially tore apart fetal mouse palates after fusion and cultivated them in culture medium with or without mouse or human amniotic fluid. We thereby found that the wounded palatal edge became completely covered with flattened epithelium after 36 hours in culture with amniotic fluid, but not in culture without amnioticfluid. Using histological and scanning electron microscopic analyses of the healing process, it was revealed that the epithelium covering the wound was almost exclusively derived from the adjacent nasal epithelium, but not from the oral epithelium. Such actions of amniotic fluid on the fetal wound were never simulated by exogenous epidermal growth factor (EGF), albumin, or both. In addition, the rapid epithelialization induced by amniotic fluid was not prevented by either PD168393 (an inhibitor of the EGF receptor-specific tyrosine kinase) or SB431542 (a specific inhibitor of TGFbeta receptor type I/ALK5). The present study provides new insights into the unique biological actions of amniotic fluid in the repair of injured fetal palate.
机译：继发pa裂是人类最常见的先天性先天缺陷之一。 left裂形成的主要原因是双侧shelves架子融合失败，但是曾经融合的pa破裂也被建议在子宫内发生。人体融合后破裂的可能性几乎没有被接受，主要是因为在所有c裂病例中，c裂边缘总是被完整的上皮覆盖。为了验证当融合的颚裂被撕开时胎儿的子宫内环境是否在伤口愈合中起作用，我们在融合后人工撕开胎儿小鼠的上颚，并在有或没有小鼠或人羊水的培养基中进行培养。因此，我们发现在羊水培养36小时后，受伤的pa边缘完全被扁平的上皮所覆盖，但在没有羊水的培养中则没有。使用组织学和扫描电子显微镜分析愈合过程，发现覆盖伤口的上皮几乎完全来自相邻的鼻腔上皮，而不是口腔上皮。羊水对胎儿伤口的这种作用从未通过外源性表皮生长因子（EGF），白蛋白或两者来模拟。此外，PD168393（一种EGF受体特异性酪氨酸激酶的抑制剂）或SB431542（一种TGFbeta受体I / ALK5的特异性抑制剂）也不能阻止羊水引起的快速上皮化。本研究提供了新的见解，羊水在修复胎儿fe中的独特生物学作用。

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