Premium
Human glial‐restricted progenitors survive, proliferate, and preserve electrophysiological function in rats with focal inflammatory spinal cord demyelination
Author(s) -
Walczak Piotr,
All Angelo H.,
Rumpal Nidhi,
Gorelik Michael,
Kim Heechul,
Maybhate Anil,
Agrawal Gracee,
Campanelli James T.,
Gilad Assaf A.,
Kerr Douglas A.,
Bulte Jeff W. M.
Publication year - 2011
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.21119
Subject(s) - remyelination , biology , spinal cord , transplantation , neuroscience , progenitor cell , neuroglia , progenitor , immunology , pathology , stem cell , central nervous system , myelin , medicine , microbiology and biotechnology
Abstract Transplantation of glial progenitor cells results in transplant‐derived myelination and improved function in rodents with genetic dysmyelination or chemical demyelination. However, glial cell transplantation in adult CNS inflammatory demyelinating models has not been well studied. Here we transplanted human glial‐restricted progenitor (hGRP) cells into the spinal cord of adult rats with inflammatory demyelination, and monitored cell fate in chemically immunosuppressed animals. We found that hGRPs migrate extensively, expand within inflammatory spinal cord lesions, do not form tumors, and adopt a mature glial phenotype, albeit at a low rate. Human GRP‐transplanted rats, but not controls, exhibited preserved electrophysiological conduction across the spinal cord, though no differences in behavioral improvement were noted between the two groups. Although these hGRPs myelinated extensively after implantation into neonatal shiverer mouse brain, only marginal remyelination was observed in the inflammatory spinal cord demyelination model. The low rate of transplant‐derived myelination in adult rat spinal cord may reflect host age, species, transplant environment/location, and/or immune suppression regime differences. We conclude that hGRPs have the capacity to myelinate dysmyelinated neonatal rodent brain and preserve conduction in the inflammatory demyelinated adult rodent spinal cord. The latter benefit is likely dependent on trophic support and suggests further exploration of potential of glial progenitors in animal models of chronic inflammatory demyelination. © 2010 Wiley‐Liss, Inc.