The Role of Fas-Mediated Apoptosis After Traumatic Spinal Cord Injury
The Role of Fas-Mediated Apoptosis After Traumatic Spinal Cord Injury
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DOI：
10.1097/01.brs.0000129894.34550.48
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发表时间：
2004-07
期刊：
影响因子：
3
通讯作者：
O. Yoshino;H. Matsuno;Hiroshi Nakamura;K. Yudoh;Yumiko Abe;T. Sawai;M. Uzuki;S. Yonehara;Tomoatsu Kimura
中科院分区：
文献类型：
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作者：
O. Yoshino;H. Matsuno;Hiroshi Nakamura;K. Yudoh;Yumiko Abe;T. Sawai;M. Uzuki;S. Yonehara;Tomoatsu Kimura
研究设计.观察Fas基因缺陷小鼠和野生型小鼠脊髓损伤后的功能恢复和组织病理学变化。目标.探讨Fas/Fas配体（FasL）系统在脊髓损伤后细胞凋亡中的作用。背景日期摘要。脊髓损伤后观察到的细胞凋亡作为最初损伤后附带损伤的原因最近引起了广泛的兴趣。Fas抗原介导的脑或脊髓缺血后细胞凋亡的报告。近年来，脊髓损伤后Fas表达上调也有报道。然而，Fas介导的细胞凋亡对继发性脊髓损伤程度的影响尚未明确。方法.我们研究了脊髓损伤后Fas介导的细胞凋亡，并使用MRL/Mp-lpr/lpr（MRL/lpr）小鼠（Fas缺陷型突变小鼠）和MRL/Mp-+/+（MRL/+）小鼠（Fas阳性野生型小鼠）检查脊髓损伤后的行为学变化和组织病理学变化。结果MRL/lpr小鼠脊髓损伤后的运动恢复上级优于MRL/+小鼠。此外，MRL/lpr小鼠的损伤面积显著小于MRL/+小鼠。此外，MRL/lpr小鼠损伤脊髓中凋亡细胞的频率显著低于MRL/+小鼠。结论我们证明了Fas介导的细胞凋亡的出现在脊髓损伤后的脊髓。此外，我们首次阐明了脊髓损伤后Fas介导的细胞凋亡在脊髓损伤和最终神经系统损伤中的重要作用。
Study Design. Functional recovery and histopathological change after spinal cord injury in the Fas-deficient mice and the wild-type mice were investigated. Objectives. To investigate the role of the Fas/Fas ligand (FasL) system as a signal transduction pathway leading to apoptosis after spinal cord injury. Summary of Background Date. Apoptosis observed after spinal cord injury has recently gained widespread interest as a cause of collateral damage after the initial injury. Apoptosis mediated by the Fas antigen in the postischemic brain or spinal cord was reported. Recently, the upregulation of Fas after spinal cord injury was also reported. However, the influence of Fas-mediated apoptosis on the extent of the secondary spinal cord injury has not yet been clarified. Methods. We investigated Fas-mediated apoptosis after spinal cord injury and examined the behavioral changes and the histopathological changes after spinal cord injury using MRL/Mp-lpr/lpr (MRL/lpr) mice, which were Fas-deficient mutant mice, and MRL/Mp-+/+ (MRL/+) mice, which were Fas-positive wild-type mice. Results. Locomotor recovery after spinal cord injury in MRL/lpr mice was superior to that observed in MRL/+ mice. In addition, the damaged area in MRL/lpr mice was significantly smaller than that seen in MRL/+ mice. Further, the frequency of apoptotic cells in the injured spinal cord of MRL/lpr mice was significantly less than that in MRL/+ mice. Conclusion. We demonstrated the appearance of Fas-mediated apoptosis in the spinal cord after spinal cord injury. In addition, we elucidated for the first time that Fas-mediated apoptosis following spinal cord injury played an important role in the spinal cord damage and the ultimate neurologic injury.