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E-cadherin promotes retinal ganglion cell neurite outgrowth in a Protein Tyrosine Phosphatase-mu dependent manner

机译:E-钙粘蛋白以蛋白酪氨酸磷酸酶-mu依赖性方式促进视网膜神经节细胞神经突生长

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摘要

During development of the visual system, retinal ganglion cells (RGCs) require cell-cell adhesion molecules and extracellular matrix proteins for axon growth. In this study, we demonstrate that the classical cadherin, E-cadherin, is expressed in RGCs from E6 to E12 and promotes neurite outgrowth from all regions of the chick retina at E6, E8 and E10. E-cadherin is also expressed in the optic tectum. E-cadherin adhesion blocking antibodies specifically inhibit neurite outgrowth on an E-cadherin substrate. The receptor-type protein tyrosine phosphatase, PTPμ, associates with E-cadherin. In this manuscript, we demonstrate that antisense-mediated down regulation of PTPμ, overexpression of catalytically inactive PTPμ, and perturbation of endogenous PTPμ using a specific PTPμ inhibitor peptide results in a substantial reduction in neurite outgrowth on E-cadherin. Taken together these findings demonstrate that E-cadherin is an important adhesion molecule for chick RGC neurite outgrowth and suggest that PTPμ expression and catalytic activity are required for outgrowth on an E-cadherin substrate.
机译:在视觉系统发育过程中,视网膜神经节细胞(RGC)需要细胞-细胞粘附分子和细胞外基质蛋白才能促进轴突生长。在这项研究中,我们证明了经典的钙粘着蛋白E-钙粘着蛋白在从E6到E12的RGC中表达,并促进了E6,E8和E10处小鸡视网膜所有区域的神经突生长。 E-钙黏着蛋白也表达在视皮质中。 E-cadherin粘附阻断抗体特异性抑制E-cadherin底物上的神经突生长。受体型蛋白酪氨酸磷酸酶PTPμ与E-钙粘蛋白结合。在本手稿中,我们证明了反义介导的PTPμ的下调,催化无活性PTPμ的过表达以及使用特定PTPμ抑制剂肽引起的内源性PTPμ的扰动会导致E-钙粘着蛋白上神经突的长大减少。综上所述,这些结果表明E-钙粘蛋白是雏鸡RGC神经突生长的重要粘附分子,并暗示PTPμ表达和催化活性是在E-钙粘蛋白底物上生长所必需的。

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