Reduction of EphA4 receptor expression after spinal cord injury does not induce axonal regeneration or return of tcMMEP response
Reduction of EphA4 receptor expression after spinal cord injury does not induce axonal regeneration or return of tcMMEP response
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DOI：
10.1016/j.neulet.2007.03.015
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发表时间：
2007-05-11
影响因子：
2.5
通讯作者：
Miranda, Jorge D.
中科院分区：
文献类型：
--
作者：
Cruz-Orengo, Lillian;Figueroa, Johnny D.;Miranda, Jorge D.
脊髓损伤（SCI）引起抑制因子的增加，这可能限制创伤后轴突的生长。在过去的十年中，Eph受体和ephrin配体已经成为已知参与神经突生长、突触形成和发育过程中轴突寻路的关键排斥信号。考虑到SCL后不允许轴突再生的环境，我们质疑具有轴突生长排斥活性的EphA4受体的表达增强是否可能导致再生失败。为了证实这一可能性，我们检测了成年大鼠挫裂性脊髓损伤后EphA4的表达。EphA4的表达研究显示EphA4蛋白具有时间依赖性，而p -肌动蛋白没有改变。EphA4在初始阶段下调，损伤后7天上调。用反义寡核苷酸阻断EphA4上调不会产生解剖或生理反应，分别用顺行示踪研究或经颅磁运动诱发电位（tcMMEP）监测。这些结果表明，创伤后EphA4受体的上调与轴突再生或损伤部位神经传导的恢复无关。2007爱思唯尔爱尔兰有限公司版权所有。
Spinal cord injury (SCI) causes an increase of inhibitory factors that may restrict axonal outgrowth after trauma. During the past decade, the Eph receptors and ephrin ligands have emerged as key repulsive cues known to be involved in neurite outgrowth, synapse formation, and axonal pathfinding during development. Given the non-permissive environment for axonal regeneration after SCL we questioned whether enhanced-expression of the EphA4 receptor with repulsive activity for axonal outgrowth is potentially responsible for the regenerative failure. To address this possibility, we have examined the expression of EphA4 after SCI in adult rats following a contusion SCI. EphA4 expression studies demonstrated a time-dependent change for EphA4 protein without alterations in P-actin. EphA4 was downregulated initially and upregulated 7 days after injury. Blockade of EphA4 upregulation with antisense oligonucleotides did not produce an anatomical or physiological response monitored with anterograde tracing studies or transcranial magnetic motor evoked potentials (tcMMEP), respectively. These results demonstrated that upregulation of EphA4 receptors after trauma is not related to axonal regeneration or return of nerve conduction across the injury site. (c) 2007 Elsevier Ireland Ltd. All rights reserved.