Effects of axon degeneration on oligodendrocyte lineage cells: dorsal rhizotomy evokes a repair response while axon degeneration rostral to spinal contusion induces both repair and apoptosis.
Effects of axon degeneration on oligodendrocyte lineage cells: dorsal rhizotomy evokes a repair response while axon degeneration rostral to spinal contusion induces both repair and apoptosis.
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DOI：
10.1002/glia.21009
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发表时间：
2010-08-15
期刊：
影响因子：
6.2
通讯作者：
Beattie, Michael S.
中科院分区：
文献类型：
--
作者：
Sun, Fang;Lin, Chien-Liang Glenn;Mctigue, Dana;Shan, Xiu;Tovar, C. Amy;Bresnahan, Jacqueline C.;Beattie, Michael S.
关键词：
脊髓损伤 (SCI) 后背柱 (DC) 的华勒变性与小胶质细胞激活和长期少突胶质细胞 (OL) 凋亡有关，这可能导致 SCI 后脱髓鞘和功能障碍。但是，SCI 后 OL 谱系细胞增加，这可能代表修复反应，并且有证据表明 SCI 后髓鞘再生。为了评估轴突变性本身在 OL 凋亡和增殖中的作用，我们切除了 L2-S2 背根，在 DC 中产生大量轴突变性和小胶质细胞激活，并且没有发现 OL 丢失或凋亡的证据。相反，NG2 和 APC (CC1) 阳性的 OL 谱系细胞数量增加，BrdU 研究表明新的 OL 形成。然后，我们测试了挫伤性 SCI (cSCI)，在 8 天时，该损伤会导致 DC 喙部出现与损伤、小胶质细胞激活和 DC OL 凋亡相当的退化。 NG2+细胞增殖和少突胶质细胞生成见于神经根切断术后。增殖和凋亡结合的最终结果是 DC OL 减少，这证实了早期的研究。使用抗氧化核酸的抗体，我们发现 cSCI 嘴侧的 OL 中发生快速且延长的 RNA 氧化，但没有证据表明 DC OL 中神经根切断后存在氧化应激。这些结果表明与轴突变性相关的信号足以诱导 OL 增殖，并且与中枢 SCI 相关的继发性损伤过程（包括氧化应激）而不是轴突变性本身是导致 OL 凋亡的原因。
Wallerian degeneration in the dorsal columns (DC) after spinal cord injury (SCI) is associated with microglial activation and prolonged oligodendrocyte (OL) apoptosis that may contribute to demyelination and dysfunction after SCI. But, there is an increase in OL lineage cells after SCI that may represent a reparative response, and there is evidence for remyelination after SCI. To assess the role of axonal degeneration per se in OL apoptosis and proliferation, we cut the L2-S2 dorsal roots producing massive axonal degeneration and microglial activation in the DC, and found no evidence of OL loss or apoptosis. Rather, the numbers of OL-lineage cells positive for NG2 and APC (CC1) increased, and BrdU studies suggested new OL formation. We then tested contusion SCI (cSCI) that results in comparable degeneration in the DC rostral to the injury, microglial activation, and apoptosis of DC OLs by 8 days. NG2+ cell proliferation and oligodendrogenesis was seen as after rhizotomy. The net result of this combination of proliferation and apoptosis was a reduction in DC OLs, confirming earlier studies. Using an antibody to oxidized nucleic acids, we found rapid and prolonged RNA oxidation in OLs rostral to cSCI, but no evidence of oxidative stress in DC OLs after rhizotomy. These results suggest that signals associated with axonal degeneration are sufficient to induce OL proliferation, and that secondary injury processes associated with the central SCI, including oxidative stress, rather than axonal degeneration per se, are responsible for OL apoptosis.
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