EXTRACELLULAR-MATRIX MOLECULES AND CELL-ADHESION MOLECULES INDUCE NEURITES THROUGH DIFFERENT MECHANISMS
EXTRACELLULAR-MATRIX MOLECULES AND CELL-ADHESION MOLECULES INDUCE NEURITES THROUGH DIFFERENT MECHANISMS
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DOI：
10.1083/jcb.111.6.2725
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发表时间：
1990-12-01
影响因子：
7.8
通讯作者：
JHABVALA, P
中科院分区：
文献类型：
--
作者：
BIXBY, JL;JHABVALA, P
最近已经清楚的是，细胞外基质（ECM）糖蛋白和各种细胞粘附分子（CAMs）都可以促进原代神经元的神经突生长，尽管对这些信号转导的细胞内机制知之甚少。我们之前已经获得证据表明，蛋白激酶C功能是神经元对层粘连蛋白反应的重要组成部分（Bixby， J. L. 1989）。神经元。3:287 - 297)。因为像L1这样的cam （Lagenauer， C, and V. Lemmon, 1987）。Proc。国家的。学会科学。美国。张丽娟，张丽娟，张丽娟。2006。我们现在已经测试了对CAMs的反应是否同样依赖于蛋白激酶C。我们发现，抑制蛋白激酶C会抑制纤维连接蛋白或胶原蛋白以及层粘连蛋白的生长。相反，C激酶抑制实际上增强了对L1或n -钙粘蛋白的初始生长反应。然而，这两种cam的生长的后期“阶段”受到抑制。此外，当使用最佳层粘连蛋白浓度时，phorbol酯对神经突生长没有影响，即使在最佳L1或n -钙粘蛋白浓度下，它也能促进神经突的生长。结果表明，与CAM底物相比，在ECM底物上的初始过程生长过程中，不同的细胞内机制起作用，并且表明蛋白激酶C的功能是这些糖蛋白上的神经突持续生长所必需的。
It has recently become clear that both extracellular matrix (ECM) glycoproteins and various cell adhesion molecules (CAMs) can promote neurite outgrowth from primary neurons, though little is known of the intracellular mechanisms through which these signals are transduced. We have previously obtained evidence that protein kinase C function is an important part of neuronal response to laminin (Bixby, J. L. 1989. Neuron. 3:287-297). Because such CAMs as L1 (Lagenauer, C., and V. Lemmon. 1987. Proc. Natl. Acad. Sci. USA. 84:7753-7757) and N-cadherin (Bixby, J. L. and R. Zhang. 1990. J. Cell Biol. 110:1253-1260) can be purified and used as substrates to promote neurite growth, we have now tested whether the response to CAMs is similarly dependent on protein kinase C. We find that inhibition of protein kinase C inhibits growth on fibronectin or collagen as well as on laminin. In contrast, C kinase inhibition actually potentiates the initial growth response to L1 or N-cadherin. The later "phase" of outgrowth on both of these CAMs is inhibited, however. Additionally, phorbol esters, which have no effect on neurite growth when optimal laminin concentrations are used, potentiate growth even on optimal concentrations of L1 or N-cadherin. The results indicate that different intracellular mechanisms operate during initial process outgrowth on ECM substrates as compared to CAM substrates, and suggest that protein kinase C function is required for continued neurite growth on each of these glycoproteins.