Amniotic fluid induces rapid epithelialization in the experimentally ruptured fetal mouse palate - implications for fetal wound healing
Amniotic fluid induces rapid epithelialization in the experimentally ruptured fetal mouse palate - implications for fetal wound healing
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DOI：
10.1387/ijdb.062216tt
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发表时间：
2007-01-01
影响因子：
0.7
通讯作者：
Shiota, Kohei
中科院分区：
文献类型：
--
作者：
Takigawa, Toshiya;Shiota, Kohei
继发性腭裂是人类最常见的先天性出生缺陷之一。腭裂形成的主要原因是两侧腭架融合失败，但曾经融合的腭也被认为在子宫内发生破裂。人类腭裂融合后破裂的可能性几乎没有被接受，主要是因为在所有腭裂病例中，腭裂边缘总是覆盖着完整的上皮。为了验证胎儿的宫内环境是否在伤口愈合中起作用，当曾经融合的腭被撕裂时，我们在融合后人工撕裂胎鼠腭，并在含有或不含小鼠或人羊水的培养基中培养它们。因此，我们发现，在羊水中培养36小时后，受伤的腭缘完全被扁平的上皮覆盖，而在无羊水的培养中则不然。使用愈合过程的组织学和扫描电子显微镜分析，发现覆盖伤口的上皮几乎完全来自邻近的鼻上皮，但不是来自口腔上皮。羊水对胎儿伤口的这种作用从未被外源性表皮生长因子（EGF）、白蛋白或两者所模拟。此外，羊水诱导的快速上皮形成不能被PD 168393（EGF受体特异性酪氨酸激酶抑制剂）或SB 431542（TGF β受体I型/ALK 5特异性抑制剂）阻止。本研究提供了新的见解独特的生物作用，羊水在修复受损的胎儿腭。
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.