Apoptosis and delayed degeneration after spinal cord injury in rats and monkeys
Apoptosis and delayed degeneration after spinal cord injury in rats and monkeys
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DOI：
10.1038/nm0197-73
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发表时间：
1997-01-01
期刊：
影响因子：
82.9
通讯作者：
Beattie, MS
中科院分区：
文献类型：
--
作者：
Crowe, MJ;Bresnahan, JC;Beattie, MS
细胞凋亡是一种形态学定义的程序性细胞死亡形式，见于各种情况，包括免疫细胞选择、癌发生和发展（1，2）。最近在中枢神经系统（CNS）缺血性或创伤性损伤后观察到细胞凋亡（3-5），表明主动细胞死亡以及被动坏死可能介导CNS损伤后的损伤。大鼠脊髓损伤（SCI）后出现典型的创伤后坏死，但在伤后6 h ~ 3周内，脊髓组织中出现凋亡细胞，尤其是脊髓白色物质。凋亡细胞的少突胶质细胞标记阳性。猴脊髓损伤后，在远端变性纤维束内发现凋亡细胞。脊髓损伤部位的继发性变性和远离损伤的神经束的慢性脱髓鞘似乎部分是由于细胞凋亡。由于细胞因子已显示在体外介导少突胶质细胞死亡（6），因此CNS损伤后的慢性脱髓鞘似乎与慢性退行性疾病（如多发性硬化症）具有共同特征。
Apoptosis is a morphologically defined form of programmed cell death seen in a variety of circumstances, including immune cell selection, carcinogenesis and development(1,2). Apoptosis has very recently been seen after ischemic or traumatic injury to the central nervous system (CNS)(3-5), suggesting that active cell death as well as passive necrosis may mediate damage after CNS injury. After spinal cord injury (SCI) in the rat, typical post-traumatic necrosis occurred, but in addition, apoptotic cells were found from 6 hours to 3 weeks after injury, especially in the spinal white matter. Apoptotic cells were positive for oligodendrocyte markers. After SCI in monkeys, apoptotic cells were found within remote degenerating fiber tracts. Both secondary degeneration at the site of SCI and the chronic demyelination of tracts away from the injury appear to be due in part to apoptosis. As cytokines have been shown to mediate oligodendrocyte death in vitro(6), it seems likely that chronic demyelination after CNS injury shares features with chronic degenerative disorders like multiple sclerosis.