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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Modulation of Receptor Protein Tyrosine Phosphatase Sigma Increases Chondroitin Sulfate Proteoglycan Degradation through Cathepsin B Secretion to Enhance Axon Outgrowth
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Modulation of Receptor Protein Tyrosine Phosphatase Sigma Increases Chondroitin Sulfate Proteoglycan Degradation through Cathepsin B Secretion to Enhance Axon Outgrowth

机译：受体蛋白酪氨酸磷酸酶Sigma的调节增加了通过组织蛋白酶B分泌通过组织蛋白酶分泌降解的软骨素蛋白多糖降解，以增强Axon Forgrowth

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摘要

Severed axon tips reform growth cones following spinal cord injury that fail to regenerate, in part, because they become embedded within an inhibitory extracellular matrix. Chondroitin sulfate proteoglycans (CSPGs) are the major axon inhibitory matrix component that is increased within the lesion scar and in perineuronal nets around deafferented neurons. We have recently developed a novel peptide modulator (intracellular sigma peptide) of the cognate receptor of CSPGs, protein tyrosine phosphatase sigma (RPTP sigma), which has been shown to markedly improve sensorimotor function, micturition, and coordinated locomotor behavior in spinal cord contused rats. However, the mechanism(s) underlying how modulation of RPTP sigma mediates axon outgrowth through inhibitory CSPGs remain unclear. Here, we describe how intracellular sigma peptide modulation of RPTP sigma induces enhanced protease Cathepsin B activity. Using DRG neurons from female Sprague Dawley rats cultured on an aggrecan/laminin spot assay and a combination of biochemical techniques, we provide evidence suggesting that modulation of RPTP sigma regulates secretion of proteases that, in turn, relieves CSPG inhibition through its digestion to allow axon migration though proteoglycan barriers. Understanding the mechanisms underlying RPTP sigma modulation elucidates how axon regeneration is impaired by proteoglycans but can then be facilitated following injury.
机译：切断的轴突尖端改性生长锥在脊髓损伤后未能再生，部分原因是它们嵌入抑制性细胞外基质中。硫酸软骨素硫酸盐蛋白多糖（CSPG）是主要的轴突抑制基质组分，其在病变瘢痕内和脱颈椎神经元周围的危险网内增加。我们最近开发了CSPGS的同源受体的新型肽调节剂（细胞内Sigma肽），蛋白酪氨酸磷酸酶Sigma（RPTP Sigma）已被证明可以显着提高脊髓污染的大鼠中的感觉运动函数，喷射和协调的运动行为。 。然而，依赖于RPTP Sigma的调节方法的机制通过抑制性CSPGS介导Axon产物仍然不清楚。在这里，我们描述了RPTP Sigma的细胞内Sigma肽调节如何诱导增强蛋白酶组织蛋白酶B活性。利用来自女性Sprague Dawley大鼠的DRG神经元在蛋白质/层膜蛋白的测定和生化技术的组合中，提出了RPTP Sigma调节蛋白酶的分泌，反过来通过其消化来调节蛋白酶的分泌，以便通过其消化来缓解CSPG抑制以允许轴突抑制CSPG抑制虽然蛋白质组成障碍障碍迁移。理解RPTP Sigma调制的机制阐明了蛋白质糖蛋白酶多糖损害的轴突再生如何，但可以在损伤后促进。

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