Increased stem cell proliferation in the spinal cord of adult amyotrophic lateral sclerosis transgenic mice

被引:40
作者
Guan, Ying-Jun
Wang, Xin
Wang, Hong-Yan
Kawagishi, Kyutaro
Ryu, Hoon
Huo, Chun-Feng
Shimony, Ethan M.
Kristal, Bruce S.
Kuhn, Hans-Georg
Friedlander, Robert M. [1 ]
机构
[1] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Neurosurg,Neuroapoptosis Lab, Boston, MA 02115 USA
[2] Weifang Med Coll, Shandong, Peoples R China
[3] Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Gothenburg, Sweden
[4] Shinshu Univ, Sch Med, Dept Anat, Matsumoto, Nagano 390, Japan
[5] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA
[6] Boston Univ, Sch Med, Dept Pathol, Boston, MA 02118 USA
[7] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA
关键词
amyotrophic lateral sclerosis; apoptosis; proliferation; spinal cord; stem cell; transgenic mice;
D O I
10.1111/j.1471-4159.2007.04610.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
Harnessing the regenerative potential of the central nervous system to repopulate depleted cellular populations from endogenous stem cells would be a novel approach for the treatment of neurological diseases resulting from cell death. We demonstrate that there is significantly increased gliogenesis, but an absence of convincing neurogenesis. The fact that the neurodegenerative process stimulates a regenerative response suggests that the adult spinal cord has at least limited ability for regeneration. Further studies will determine if Consequently, understanding if and how the central nervous this endogenous regenerative process can be enhanced and system is capable of such regeneration would determine if such an approach is feasible. In this report, we provide evidence of widespread regenerative response in the spinal cord of amyotrophic lateral sclerosis transgenic mice. However, this regenerative response appears to be largely unproductive. directed so as to slow or even reverse the natural progression of this devastating disease.
引用
收藏
页码:1125 / 1138
页数:14
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