The myelin-associated glycoprotein (MAG) has been postulated to play a crucial role during myelin formation. Evidence supporting this hypothesis was provided by infecting rat Schwann cells with a retrovirus expressing MAG antisense RNA; these Schwann cells showed reduced levels of MAG expression and
Microglia enhance dorsal root ganglion outgrowth in Schwann cell cultures
✍ Scribed by Dianna L. Hynds; Nagarathnamma Rangappa; Julia Ter Beest; Diane M. Snow; Alexander G. Rabchevsky
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 405 KB
- Volume
- 46
- Category
- Article
- ISSN
- 0894-1491
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Transplantation of cellular populations to facilitate regrowth of damaged axons is a common experimental therapy for spinal cord injury. Schwann cells (SC) or microglia grafted into injury sites can promote axonal regrowth of central projections of dorsal root ganglion (DRG) sensory neurons. We sought to determine whether the addition of microglia or microglia‐derived secretory products alters DRG axon regrowth upon cultures of SC. Rat DRG explants were grown on monolayers consisting of either SC, microglia, SC exposed to microglia‐conditioned medium (MCM), or co‐cultures with different relative concentrations of microglia. Image analysis revealed that, compared to SC alone, the extent of neurite outgrowth was significantly greater on SC‐microglia co‐cultures. Immunocytochemistry for extracellular matrix molecules showed that microglial cells stained positively for growth‐promoting thrombospondin, whereas laminin and the inhibitory chondroitin sulfate proteoglycans (CSPGs) were localized primarily to SC. Notably, immunoreactivity for CSPGs appeared reduced in areas associated with DRG outgrowth in co‐cultures and SC exposed to MCM. These results show that microglia or their secreted products can augment SC‐mediated DRG regrowth in vitro, indicating that co‐grafting SC with microglia provides a novel approach to augment sensory fiber regeneration after spinal cord injury. © 2004 Wiley‐Liss, Inc.
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