Unilateral induction of progenitors in the spinal cord of hSOD1G93A transgenic rats correlates with an asymmetrical hind limb paralysis

被引:12
|
作者
de Hemptinne, Isabelle
Boucherie, Cedric
Pochet, Roland
Bantubungi, Kadiombo
Schiffmann, Serge N.
Maloteaux, Jean-Marie
Hermans, Emmanuel
机构
[1] Catholic Univ Louvain, Lab Pharmacol Expt, B-1200 Brussels, Belgium
[2] Univ Libre Bruxelles, Fac Med, Lab Histol Neuroanat & Neuropathol, Brussels, Belgium
[3] Univ Libre Bruxelles, Fac Med, Neurophysiol Lab, Brussels, Belgium
关键词
amyotrophic lateral sclerosis; hSOD1(G93A); stem cell factor; nestin; c-Kit;
D O I
10.1016/j.neulet.2006.02.060
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Transgenic rats expressing a mutated form of the human Cu/Zn superoxide dismutase (hSOD1(G93A)) develop an amyotrophic lateral sclerosis (ALS)-like phenotype, including motor neurone degeneration and reactive gliosis in the spinal cord. This study aimed at examining the presence of endogenous neural progenitors in the lumbar spinal cord of these rats at the end-stage of the disease. Immunohistochemical data clearly demonstrated the induced expression of the stem cell factor reported as a chemoattractant and survival factor for neural stem cells as well as nestin (neuro-epithelial stem cell intermediate filament) in the spinal cord sections. While the stem cell factor immunolabelling appeared diffuse throughout the gray matter, nestin labelling was restricted to clusters within the ventral horn. Interestingly, as paralysis regularly develops asymmetrically, induction of nestin was only detected on the ipsilateral side of the predominant symptoms. Finally, immunohistochemical detection of the stem cell factor receptor (c-Kit) revealed its specific induction which coincided with nestin immunolabelling. Together, these results are indicative of endogenous recruitment of neural progenitors within lesioned tissues and could support the development of treatments involving endogenous or exogenous stem cells. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:25 / 29
页数:5
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