Daniloff J K, Crossin K L, Pinçon-Raymond M, Murawsky M, Rieger F, Edelman G M
Rockefeller University, New York 10021.
J Cell Biol. 1989 Feb;108(2):625-35. doi: 10.1083/jcb.108.2.625.
Cytotactin is an extracellular glycoprotein found in a highly specialized distribution during embryonic development. In the brain, it is synthesized by glia, not neurons. It is involved in neuron-glia adhesion in vitro and affects neuronal migration in the developing cerebellum. In an attempt to extend these observations to the peripheral nervous system, we have examined the distribution and localization of cytotactin in different parts of the normal and regenerating neuromuscular system. In the normal neuromuscular system, cytotactin accumulated at critical sites of cell-cell interactions, specifically at the neuromuscular junction and the myotendinous junction, as well at the node of Ranvier (Rieger, F., J. K. Daniloff, M. Pinçon-Raymond, K. L. Crossin, M. Grumet, and G. M. Edelman. 1986. J. Cell Biol. 103:379-391). At the neuromuscular junction, cytotactin was located in terminal nonmyelinating Schwann cells. Cytotactin was also detected near the insertion points of the muscle fibers to tendinous structures in both the proximal and distal endomysial regions of the myotendinous junctions. This was in striking contrast to staining for the neural cell adhesion molecule, N-CAM, which was accumulated near the extreme ends of the muscle fiber. Peripheral nerve damage resulted in modulation of expression of cytotactin in both nerve and muscle, particularly among the interacting tissues during regeneration and reinnervation. In denervated muscle, cytotactin accumulated in interstitial spaces and near the previous synaptic sites. Cytotactin levels were elevated and remained high along the endoneurial tubes and in the perineurium as long as muscle remained denervated. Reinnervation led to a return to normal levels of cytotactin both in inner surfaces of the nerve fascicles and in the perineurium. In dorsal root ganglia, the processes surrounding ganglionic neurons became intensely stained by anticytotactin antibodies after the nerve was cut, and returned to normal by 30 d after injury. These data suggest that local signals between neurons, glia, and supporting cells may regulate cytotactin expression in the neuromuscular system in a fashion coordinate with other cell adhesion molecules. Moreover, innervation may regulate the relative amount and distribution of cytotactin both in muscle and in Schwann cells.
细胞趋触蛋白是一种细胞外糖蛋白，在胚胎发育过程中以高度特化的方式分布。在大脑中，它由神经胶质细胞而非神经元合成。它在体外参与神经元与神经胶质细胞的黏附，并影响发育中小脑的神经元迁移。为了将这些观察结果扩展到外周神经系统，我们研究了细胞趋触蛋白在正常和再生神经肌肉系统不同部位的分布和定位。在正常神经肌肉系统中，细胞趋触蛋白聚集在细胞间相互作用的关键部位，特别是在神经肌肉接头和肌腱连接部位，以及郎飞结处（里格，F.，J.K. 达尼洛夫，M. 潘松 - 雷蒙德，K.L. 克罗辛，M. 格鲁梅特，和 G.M. 埃德尔曼。1986年。《细胞生物学杂志》103:379 - 391）。在神经肌肉接头处，细胞趋触蛋白位于终末无髓鞘施万细胞中。在肌腱连接部位的近端和远端肌内膜区域，在肌纤维与肌腱结构的插入点附近也检测到了细胞趋触蛋白。这与神经细胞黏附分子N - CAM的染色形成了鲜明对比，N - CAM聚集在肌纤维的极端末端附近。外周神经损伤导致神经和肌肉中细胞趋触蛋白表达的调节，特别是在再生和再支配过程中相互作用的组织中。在失神经支配的肌肉中，细胞趋触蛋白聚集在间隙空间和先前突触部位附近。只要肌肉保持失神经支配状态，细胞趋触蛋白水平在神经内膜管和神经束膜中就会升高并维持在高位。再支配导致神经束膜内表面和神经束膜中细胞趋触蛋白水平恢复正常。在背根神经节中，切断神经后，围绕神经节神经元的突起被抗细胞趋触蛋白抗体强烈染色，并在损伤后30天恢复正常。这些数据表明，神经元、神经胶质细胞和支持细胞之间的局部信号可能以与其他细胞黏附分子协调的方式调节神经肌肉系统中细胞趋触蛋白的表达。此外，神经支配可能调节肌肉和施万细胞中细胞趋触蛋白的相对含量和分布。
