Meijers J H, Tibboel D, van der Kamp A W, Van Haperen-Heuts I C, Klück P, Molenaar J C
Pediatr Res. 1987 May;21(5):466-70. doi: 10.1203/00006450-198705000-00009.
Based on experimental studies in mutant mouse strains, an imbalance between the rate of migration of neural crest cells and the rate of differentiation of the mesenchyme of the distal gut has been proposed as an etiological factor in Hirschsprung's disease. We studied the influence of the stage of differentiation of embryonal chick gut on the migration of neural crest cells in an in vivo culture system: the chorioallantoic membrane. Neural crest cells in cultured gut were demonstrated with antibodies directed against the HNK-1 epitope. Enteric neurons were demonstrated with neurofilament immunoreactivity. By culturing isolated gut segments of E4 embryos, we obtained aneuronal (neurofilament-negative) embryonal chick gut up to 25 days of development. In cocultures of aneuronal gut and the neural anlage (neural tube and neural crest) neural crest cell colonization was observed, even in advanced stages of differentiation. The significance of the results is discussed in terms of the etiology of Hirschsprung's disease.
基于对突变小鼠品系的实验研究，有人提出神经嵴细胞迁移速率与远端肠道间充质分化速率失衡是先天性巨结肠病的一个病因。我们在一个体内培养系统——尿囊膜中，研究了胚胎期鸡肠道的分化阶段对神经嵴细胞迁移的影响。用针对HNK-1表位的抗体来证实培养肠道中的神经嵴细胞。用神经丝免疫反应性来证实肠神经元。通过培养E4胚胎的分离肠道段，我们获得了发育至25天的无神经元（神经丝阴性）胚胎期鸡肠道。在无神经元肠道与神经原基（神经管和神经嵴）的共培养中，即使在分化的晚期阶段也观察到了神经嵴细胞的定植。从先天性巨结肠病的病因学角度对结果的意义进行了讨论。
