Leblanc G G, Holbert T E
Department of Biological Structure and Function, Oregon Health Sciences University, Portland 97201, USA.
J Neurobiol. 1996 Feb;29(2):249-61. doi: 10.1002/(SICI)1097-4695(199602)29:2<249::AID-NEU9>3.0.CO;2-A.
Different anteroposterior (AP) regions of the neural crest normally produce different cell types, both in vivo and in vitro. AP differences in neural crest cell fates appear to be specified in part by mechanisms that act prior to neural crest cell migration. We, therefore, examined the possibility that the fates of neural crest cells, like those of neural tube cells, can be regulated by interactions with Hensen's node. Using a transfilter co-culture system, we found that young (stage 3+ to 4) Hensen's node up-regulates the expression of two cranial-specific phenotypes (fibronectin and smooth muscle actin immunoreactivities) in mass cultures of trunk neural crest cells, and down-regulates the expression of a trunk-specific phenotype (melanin synthesis). The changes in phenotype produced by exposure to young Hensen's node were not accompanied by changes in the proliferation of either fibronectin immunoreactive cells or melanocytes. The capacity of Hensen's node to elicit changes in trunk neural crest cell phenotype decreased as the developmental age of the node increased and was lost by stage 6. In addition, old Hensen's node did not stimulate the expression of trunk-specific phenotypes in cranial neural crest cells, suggesting that cranial- and trunk-specific phenotypes are induced by different mechanisms.
在体内和体外，神经嵴的不同前后（AP）区域通常会产生不同的细胞类型。神经嵴细胞命运的前后差异似乎部分是由在神经嵴细胞迁移之前起作用的机制所决定的。因此，我们研究了神经嵴细胞的命运是否像神经管细胞一样，可以通过与亨森结的相互作用来调节。使用跨滤器共培养系统，我们发现年轻的（3+至4期）亨森结在躯干神经嵴细胞的大量培养中上调了两种颅特异性表型（纤连蛋白和平滑肌肌动蛋白免疫反应性）的表达，并下调了一种躯干特异性表型（黑色素合成）的表达。暴露于年轻的亨森结所产生的表型变化并未伴随着纤连蛋白免疫反应性细胞或黑素细胞增殖的变化。随着亨森结发育年龄的增加，其引发躯干神经嵴细胞表型变化的能力下降，并在6期丧失。此外，年老的亨森结不会刺激颅神经嵴细胞中躯干特异性表型的表达，这表明颅特异性和躯干特异性表型是由不同机制诱导的。
