Unilateral induction of progenitors in the spinal cord of hSOD1(G93A) transgenic rats correlates with an asymmetrical hind limb paralysis.
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.
Laboratoire de Pharmacologie Expérimentale, Université catholique de Louvain, Av. Hippocrate 54.10, B-1200 Brussels, Belgium.
Isabelle
I
de Hemptinne
Cédric
C
Boucherie
Roland
R
Pochet
Kadiombo
K
Bantubungi
Serge N
SN
Schiffmann
Jean-Marie
JM
Maloteaux
Emmanuel
E
Hermans
D000690:Amyotrophic Lateral Sclerosis / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D030801:Animals, Genetically Modified; D002454:Cell Differentiation / Q000235:genetics; D002465:Cell Movement / Q000235:genetics; D004195:Disease Models, Animal; D007839:Functional Laterality / Q000235:genetics; D006614:Hindlimb / Q000294:innervation / Q000503:physiopathology; D006801:Humans; D007150:Immunohistochemistry; D007381:Intermediate Filament Proteins / Q000378:metabolism; D009046:Motor Neurons / Q000378:metabolism; D009416:Nerve Regeneration / Q000235:genetics*; D009419:Nerve Tissue Proteins / Q000378:metabolism; D064231:Nestin; D009474:Neurons / Q000378:metabolism; D010243:Paralysis / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D051381:Rats; D020127:Recovery of Function / Q000235:genetics; D013116:Spinal Cord / Q000166:cytology / Q000378:metabolism* / Q000503:physiopathology; D019089:Stem Cell Factor / Q000378:metabolism; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000235:genetics*; D000072105:Superoxide Dismutase-1
D007381:Intermediate Filament Proteins; C577484:NES protein, human; D009419:Nerve Tissue Proteins; C577486:Nes protein, rat; D064231:Nestin; C000606290:SOD1 protein, human; D019089:Stem Cell Factor; C000606292:Sod1 protein, rat; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D019009:Proto-Oncogene Proteins c-kit