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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Inhibiting epidermal growth factor receptor attenuates reactive astrogliosis and improves functional outcome after spinal cord injury in rats
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Inhibiting epidermal growth factor receptor attenuates reactive astrogliosis and improves functional outcome after spinal cord injury in rats

机译：抑制表皮生长因子受体可减轻大鼠脊髓损伤后反应性星形胶质增生并改善功能结局

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摘要

As a physical barrier to regenerating axons, reactive astrogliosis is also a biochemical barrier which can secrete inhibitory molecules, including chondroitin sulfate proteoglycans (CSPGs) in the pathological mechanism of spinal cord injury (SCI). Thus, inhibition of astroglial proliferation and CSPG production might facilitate axonal regeneration after SCI. Recent studies have demonstrated that epidermal growth factor receptor (EGFR) activation triggers quiescent astrocytes into becoming reactive astrocytes and forming glial scar after CNS injury. In the present study, we investigated whether a specific EGFR inhibitor (AG1478) could attenuate the reactive astrogliosis and production of CSPGs, alleviate demyelination, and eventually enhance the functional recovery after SCI in rats. Our results showed that pEGFR immunoreactivity was up-regulated significantly post injury, mainly confined to astrocytes. Meanwhile, astrocytes near the injury site after SCI became activated obviously characterized by hypertrophic morphology and enhanced GFAP expression. However, administration of AG1478 remarkably reduced trauma induced-reactive astrogliosis and accumulation of CSPGs. Furthermore, the treatment with AG1478 also alleviated demyelination, increased expression of growth-associated proteins-43 (GAP-43) and improved hindlimb function after SCI. Therefore, the local blockade of EGFR in an injured area is beneficial to functional outcome by facilitating a more favorable environment for axonal regeneration in SCI rats.
机译：作为再生轴突的物理屏障，反应性星形胶质增生也是一种生化屏障，它可以在脊髓损伤（SCI）的病理机制中分泌抑制性分子，包括硫酸软骨素蛋白聚糖（CSPG）。因此，抑制星形胶质细胞增殖和CSPG的产生可能有助于脊髓损伤后轴突再生。最近的研究表明，表皮生长因子受体（EGFR）的激活触发中枢神经系统损伤后，静止的星形胶质细胞变成反应性星形胶质细胞并形成神经胶质瘢痕。在本研究中，我们研究了一种特定的EGFR抑制剂（AG1478）是否可以减轻大鼠反应性星形胶质细胞增生和CSPG的产生，减轻脱髓鞘作用并最终增强SCI大鼠的功能恢复。我们的结果表明，pEGFR免疫反应性在损伤后显着上调，主要限于星形胶质细胞。同时，SCI激活后损伤部位附近的星形胶质细胞明显具有肥大形态和增强的GFAP表达。但是，AG1478的使用显着减少了创伤诱发的反应性星形胶质增生和CSPG的积累。此外，AG1478的治疗还减轻了脱髓鞘作用，增加了SCI后生长相关蛋白43（GAP-43）的表达并改善了后肢功能。因此，通过促进SCI大鼠轴突再生的更有利环境，在受损区域中对EGFR的局部阻断有利于功能预后。

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