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
相关论文
共 50 条
  • [41] Topiramate protects against motor neuron degeneration in organotypic spinal cord cultures but not in G93A SOD1 transgenic mice
    Maragakis, NJ
    Jackson, M
    Ganel, R
    Rothstein, JD
    NEUROSCIENCE LETTERS, 2003, 338 (02) : 107 - 110
  • [42] Neuronal nitric oxide synthase (nNOS) immunoreactivity in the spinal cord of transgenic mice with G93A mutant SOD1 gene
    Shoichi Sasaki
    Hitoshi Warita
    Koji Abe
    Makoto Iwata
    Acta Neuropathologica, 2002, 103 : 421 - 427
  • [43] OECs transplantation in spinal cord prolongs the survival of mutant SOD1 (G93A) ALS rats through neuroprotection
    Zhou, Changman
    FASEB JOURNAL, 2011, 25
  • [44] Overexpression of SOD1 in transgenic rats attenuates nuclear translocation of endonuclease g and apoptosis after spinal cord injury
    Yu, Fengshan
    Sugawara, Taku
    Nishi, Tatsuro
    Liu, Jing
    Chan, Pak H.
    JOURNAL OF NEUROTRAUMA, 2006, 23 (05) : 595 - 603
  • [45] Progressive accumulation of protein nitrotyrosine in brain and spinal cord in transgenic mice bearing FALS-associated (G93A) superoxide dismutase 1
    Trifiletti, RR
    Kostic, V
    JacksonLewis, V
    Bandele, AN
    Przedborski, S
    ANNALS OF NEUROLOGY, 1997, 42 (03) : T198 - T198
  • [46] Muscle Expression of SOD1G93A Modulates microRNA and mRNA Transcription Pattern Associated with the Myelination Process in the Spinal Cord of Transgenic Mice
    Dobrowolny, Gabriella
    Bernardini, Camilla
    Martini, Martina
    Baranzini, Mirko
    Barba, Marta
    Musaro, Antonio
    FRONTIERS IN CELLULAR NEUROSCIENCE, 2015, 9 : 1 - 12
  • [47] Transgenic SOD1 G93A mice develop reduced GLT-1 in spinal cord without alterations in cerebrospinal fluid glutamate levels
    Bendotti, C
    Tortarolo, M
    Suchak, SK
    Calvaresi, N
    Carvelli, L
    Bastone, A
    Rizzi, M
    Rattray, M
    Mennini, T
    JOURNAL OF NEUROCHEMISTRY, 2001, 79 (04) : 737 - 746
  • [48] Olfactory Ensheathing Cell Transplantation Into Spinal Cord Prolongs the Survival of Mutant SOD1G93A ALS Rats Through Neuroprotection and Remyelination
    Li, Ying
    Bao, Jianling
    Khatibi, Nikan H.
    Chen, Lin
    Wang, Hongmei
    Duan, Yaokui
    Huang, Hongyun
    Zhou, Changman
    ANATOMICAL RECORD-ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, 2011, 294 (05): : 847 - 857
  • [49] Decreased GLT-1 and increased SOD1 and HO-1 expression in astrocytes contribute to lumbar spinal cord vulnerability of SOD1-G93A transgenic mice
    Guo, Yansu
    Duan, Weisong
    Li, Zhongyao
    Huang, Jing
    Yin, Yunxia
    Zhang, Kunxi
    Wang, Qian
    Zhang, Zhifang
    Li, Chunyan
    FEBS LETTERS, 2010, 584 (08): : 1615 - 1622
  • [50] Accumulation of human SOD1 and ubiquitinated deposits in the spinal cord of SOD1G93A mice during motor neuron disease progression correlates with a decrease of proteasome
    Cheroni, C
    Peviani, M
    Cascio, P
    DeBlasi, S
    Monti, C
    Bendotti, C
    NEUROBIOLOGY OF DISEASE, 2005, 18 (03) : 509 - 522