Cell proliferation and nestin expression in the ependyma of the adult rat spinal cord after injury

被引:209
作者
Namiki, J
Tator, CH
机构
[1] Univ Toronto, Toronto Hosp, Playfair Neurosci Unit, Western Div, Toronto, ON M5T 2S8, Canada
[2] Univ Toronto, Toronto Hosp, Div Neurosurg, Western Div, Toronto, ON M5T 2S8, Canada
关键词
central canal; ependyma; Ki-67; nestin; precursor cell; proliferation; spinal cord injury;
D O I
10.1097/00005072-199905000-00008
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
A population of precursor cells is known to exist in the subependyma of the lateral ventricles in adult rodents. However, the source of the precursor cells in the adult mammalian spinal cord has not been identified in vivo, although the adult spinal cord was recently reported to contain neural stem cells in vitro. In this study we found active cell proliferation and nestin expression in the adult ependyma of the central canal after spinal cord injury. The normal ependyma showed limited proliferative activity indicated by a low Ki-67 labeling index (1.5% at T1 level) and no immunoreactivity to nestin, a marker for neural precursor cells. In contrast, the spinal cord injured by clip compression demonstrated a dramatic increase in ependymal proliferation indicated by a high Ki-67 labeling index (maximum of 26% at 3 days [d] after injury) and concomitant strong nestin expression in the ependyma. These responses were downregulated by 7 d after injury. The increased cell proliferation in the ependyma was observed only at sites immediately adjacent to the lesion. After injury, nestin positive, GFAP negative cell populations were found in areas surrounding the ependymal layer, which suggests migration of the ependymal cells. These results indicate the precursor cell qualities of the adult ependyma after injury. Thus, we propose the ependyma of the central canal, which is normally latent but activates locally and temporally in response to spinal cord injury, as the in vivo source for precursor cells in the adult mammalian spinal cord.
引用
收藏
页码:489 / 498
页数:10
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