Doherty P, Cohen J, Walsh F S
Department of Experimental Pathology, UMDS, Guy's Hospital, London, England.
Neuron. 1990 Aug;5(2):209-19. doi: 10.1016/0896-6273(90)90310-c.
We have used monolayers of control 3T3 cells and 3T3 cells transfected with a cDNA encoding human N-CAM as a culture substrate for embryonic chick retinal ganglion cells (RGCs). At embryonic day 6 (E6), but not at E11, RGCs extended longer neurites on monolayers of N-CAM-transfected cells. This loss of RGC responsiveness was not associated with substantial changes in the level of N-CAM expression on RGC growth cones. The neurite outgrowth response from E6 RGCs could be inhibited by removal of N-CAM from the monolayer, by removal of alpha 2-8-linked polysialic acid from neuronal N-CAM, or by antibodies that bind exclusively to chick (neuronal) N-CAM. In contrast, the response was not dependent on neuronal beta 1 integrin function. These data provide substantive evidence for a homophilic binding mechanism directly mediating N-CAM-dependent neurite outgrowth, and suggest that changes in polysialic acid expression on neuronal N-CAM may modulate N-CAM-dependent axonal growth during development.
我们使用了对照3T3细胞单层以及转染了编码人N-细胞黏附分子（N-CAM）的cDNA的3T3细胞单层，作为胚胎鸡视网膜神经节细胞（RGCs）的培养底物。在胚胎第6天（E6），而非E11时，RGCs在N-CAM转染细胞的单层上伸出更长的神经突。RGC反应性的这种丧失与RGC生长锥上N-CAM表达水平的显著变化无关。来自E6 RGCs的神经突生长反应可通过从单层中去除N-CAM、从神经元N-CAM中去除α2-8连接的多唾液酸或通过仅与鸡（神经元）N-CAM结合的抗体来抑制。相反，该反应不依赖于神经元β1整合素功能。这些数据为直接介导N-CAM依赖性神经突生长的同源性结合机制提供了实质性证据，并表明神经元N-CAM上多唾液酸表达的变化可能在发育过程中调节N-CAM依赖性轴突生长。
