Crowe M J, Bresnahan J C, Shuman S L, Masters J N, Beattie M S
Department of Cell Biology, Neurobiology, and Anatomy, Ohio State University College of Medicine, Columbus 43210, USA.
Nat Med. 1997 Jan;3(1):73-6. doi: 10.1038/nm0197-73.
Apoptosis is a morphologically defined form of programmed cell death seen in a variety of circumstances, including immune cell selection, carcinogenesis and development. Apoptosis has very recently been seen after ischemic or traumatic injury to the central nervous system (CNS), 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, it seems likely that chronic demyelination after CNS injury shares features with chronic degenerative disorders like multiple sclerosis.
细胞凋亡是一种在多种情况下出现的程序性细胞死亡的形态学定义形式,包括免疫细胞选择、致癌作用和发育过程。最近在中枢神经系统(CNS)发生缺血性或创伤性损伤后也观察到了细胞凋亡,这表明主动细胞死亡以及被动坏死可能在中枢神经系统损伤后介导损伤。大鼠脊髓损伤(SCI)后,出现了典型的创伤后坏死,但此外,在损伤后6小时至3周内发现了凋亡细胞,尤其是在脊髓白质中。凋亡细胞对少突胶质细胞标志物呈阳性。猴子脊髓损伤后,在远处退化的纤维束中发现了凋亡细胞。脊髓损伤部位的继发性变性以及远离损伤部位的束的慢性脱髓鞘似乎部分归因于细胞凋亡。由于细胞因子已被证明在体外介导少突胶质细胞死亡,因此中枢神经系统损伤后的慢性脱髓鞘似乎与多发性硬化等慢性退行性疾病具有共同特征。