Tripathi Richa, McTigue Dana M
Department of Neuroscience, Center for Brain and Spinal Cord Repair, Ohio State University, 333 W. 10th Avenue, Columbus, OH 43210, USA.
Glia. 2007 May;55(7):698-711. doi: 10.1002/glia.20491.
Oligodendrocyte (OL) loss and axon demyelination occur after spinal cord injury (SCI). OLs may be replaced, however, by proliferating NG2+ progenitor cells. Indeed, new OLs have been noted in ventral white matter after SCI. Since tissue adjacent to lesion cavities is exposed to different mediators compared with outlying spared tissue, the authors used a rat SCI model to compare NG2 cell proliferation and OL genesis adjacent to lesion cavities with that in spared tissue closer to meninges. NG2 cells proliferated throughout the first week postinjury and accumulated along lesion borders, especially within gray matter. By 3 days postinjury (dpi), new OLs were detected throughout the cross-sections; between 4 and 7 dpi, however, oligogenesis was restricted to lesion borders. New OLs derived from cells proliferating during 1-7 dpi increased dramatically by 14 dpi; most were located along lesion borders and in spared gray matter. Oligogenesis continued along lesion borders during the second week postinjury. Overall OL numbers were reduced at 3 dpi in spared tissue, but rebounded to normal levels by 14 dpi. Surprisingly, lesion borders maintained normal OL numbers at 3 dpi, which then rose to exceed preinjury levels at 7 and 14 dpi. These results indicate that oligogenesis is protracted after SCI and leads to increased OL numbers. Most new OLs are formed in regions of greatest NG2 cell proliferation. Thus, the adult spinal cord spontaneously develops a dynamic gliogenic zone along lesion borders.
脊髓损伤（SCI）后会发生少突胶质细胞（OL）丢失和轴突脱髓鞘。然而，OLs 可能会被增殖的 NG2 + 祖细胞所替代。事实上，SCI 后在腹侧白质中已发现新的 OLs。由于与远离病变的 spared 组织相比，病变腔附近的组织会接触到不同的介质，作者使用大鼠 SCI 模型来比较病变腔附近与更靠近脑膜的 spared 组织中 NG2 细胞增殖和 OL 生成情况。损伤后第一周内 NG2 细胞持续增殖，并沿病变边界聚集，尤其是在灰质内。损伤后 3 天（dpi），在整个横切面上都检测到了新的 OLs；然而，在 4 至 7 dpi 之间，少突胶质细胞生成仅限于病变边界。由 1 - 7 dpi 期间增殖的细胞衍生而来的新 OLs 在 14 dpi 时显著增加；大多数位于病变边界和 spared 灰质中。损伤后第二周，少突胶质细胞生成在病变边界持续进行。在 spared 组织中，3 dpi 时 OL 总数减少，但到 14 dpi 时反弹至正常水平。令人惊讶的是，病变边界在 3 dpi 时保持正常的 OL 数量，然后在 7 和 14 dpi 时升至超过损伤前水平。这些结果表明，SCI 后少突胶质细胞生成过程延长，并导致 OL 数量增加。大多数新的 OLs 形成于 NG2 细胞增殖最显著的区域。因此，成年脊髓在病变边界自发形成一个动态的胶质生成区。
