SOD1 overexpression improves features of the oligodendrocyte precursor response in vitro

► Overexpression of hSOD1 increases proliferation rate and oligodendrocyte precursor cells (OPCs) in vitro. ► SOD1 overexpression in OPCs accelerates the acquisition of a mature oligodendrocyte (OL) phenotype in vitro. ► Overexpression of hSOD1 in OPCs, but not mature OLs, rescues cells from oxidati...

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Bibliographic Details
Published in:Neuroscience letters 2011-09, Vol.503 (1), p.10-14
Main Authors: Veiga, S., Ly, J., Chan, P.H., Bresnahan, J.C., Beattie, M.S.
Format: Article
Language:English
Subjects:
Analysis of Variance
Animals
Biological and medical sciences
Bromodeoxyuridine - metabolism
CD11b Antigen - metabolism
Cell Count
Cell Differentiation - drug effects
Cell Differentiation - genetics
Cell Proliferation - drug effects
Cells, Cultured
Cerebral Cortex - cytology
Dose-Response Relationship, Drug
Fundamental and applied biological sciences. Psychology
Gangliosides - metabolism
Humans
Intercellular Signaling Peptides and Proteins - pharmacology
Myelin Basic Protein - metabolism
Oligodendrocyte differentiation
Oligodendroglia - drug effects
Oligodendroglia - physiology
OPC proliferation
OPC response
Oxidative stress
Rats
Rats, Sprague-Dawley
Rats, Transgenic
Stem Cells - drug effects
Stem Cells - physiology
Superoxide dismutase
Superoxide Dismutase - genetics
Superoxide Dismutase - metabolism
Superoxide Dismutase-1
tert-Butylhydroperoxide - pharmacology
Time Factors
Vertebrates: nervous system and sense organs
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Summary:► Overexpression of hSOD1 increases proliferation rate and oligodendrocyte precursor cells (OPCs) in vitro. ► SOD1 overexpression in OPCs accelerates the acquisition of a mature oligodendrocyte (OL) phenotype in vitro. ► Overexpression of hSOD1 in OPCs, but not mature OLs, rescues cells from oxidative stress-mediated death. Spinal cord injury (SCI) produces a significant loss of oligodendrocytes (OL) and demyelination. The oligodendrocyte precursor cells (OPCs) response includes a group of cellular changes in OPCs that are directed to replenish OL loss from the injury. However, this adaptive response is hampered and OPCs eventually die or fail to differentiate to mature and functional OL. In this study, we wanted to evaluate if overexpression of human superoxide dismutase 1 (hSOD1) in OPCs from the SOD1 transgenic rat could improve some of the features of the OPC response in vitro. We found that hSOD1 overexpression increases the proliferation of OPCs and accelerates their differentiation to mature OL in vitro. Furthermore, hSOD1 overexpression reduces oxidative stress-mediated death in OPCs. These results suggest hSOD1 as a therapeutic target to increase OPC response success and potentially, OL replacement and remyelination after SCI.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2011.07.053