Object Spinal cord injury (SCI) often results in irreversible and permanent neurological deficits below the injury site and is considered a pathological state of functional damage to local neurons and axon fibers. There are several experimental treatments to minimize tissue damage, and recently cell transplantation has emerged as a promising approach in spinal cord repair. The authors undertook this study to evaluate grafting of neural tube precursors as a possible therapeutic strategy in a model of spinal cord compression in the mouse. Methods Compression SCI was induced at the T-13 level in adult male mice. Immediately after injury, neural precursor cells (NPs) were transplanted into the SCI lesion cavity in 18 mice; the remaining 19 mice received saline injections into the lesion cavity and were used as controls. Spinal cords were examined 12, 19, and 26 days postinjury to investigate the survival of the NPs and their effects on the cellular environment, glial scar and glial cyst formation, astrogliosis, and microglial activation. Results Grafted NPs survived well and integrated into the host spinal cord tissue. Some NPs had differentiated into cells expressing glial and neuronal markers at all 3 end points. Analysis of glial cyst volume showed a lesion volume reduction of 63.2% in the NP-treated mice compared with volume in the injured but untreated mice. There appeared to be no difference in astroglial and microglial activation between untreated mice and treated ones. Sensory and motor tests demonstrated that transplantation of NPs promoted improvement in injured and treated animals compared with controls. Conclusions These results support the therapeutic potential of NPs, demonstrating that they can survive for a long time, differentiate, integrate into the injured spinal cord, and promote functional recovery after SCI.

Early graft of neural precursors in spinal cord compression reduces glial cyst and improves function

BOIDO, Marina Maria;GARBOSSA, Diego;VERCELLI, Alessandro
2011-01-01

Abstract

Object Spinal cord injury (SCI) often results in irreversible and permanent neurological deficits below the injury site and is considered a pathological state of functional damage to local neurons and axon fibers. There are several experimental treatments to minimize tissue damage, and recently cell transplantation has emerged as a promising approach in spinal cord repair. The authors undertook this study to evaluate grafting of neural tube precursors as a possible therapeutic strategy in a model of spinal cord compression in the mouse. Methods Compression SCI was induced at the T-13 level in adult male mice. Immediately after injury, neural precursor cells (NPs) were transplanted into the SCI lesion cavity in 18 mice; the remaining 19 mice received saline injections into the lesion cavity and were used as controls. Spinal cords were examined 12, 19, and 26 days postinjury to investigate the survival of the NPs and their effects on the cellular environment, glial scar and glial cyst formation, astrogliosis, and microglial activation. Results Grafted NPs survived well and integrated into the host spinal cord tissue. Some NPs had differentiated into cells expressing glial and neuronal markers at all 3 end points. Analysis of glial cyst volume showed a lesion volume reduction of 63.2% in the NP-treated mice compared with volume in the injured but untreated mice. There appeared to be no difference in astroglial and microglial activation between untreated mice and treated ones. Sensory and motor tests demonstrated that transplantation of NPs promoted improvement in injured and treated animals compared with controls. Conclusions These results support the therapeutic potential of NPs, demonstrating that they can survive for a long time, differentiate, integrate into the injured spinal cord, and promote functional recovery after SCI.
2011
15
97
106
spinal cord injury; cell therapy; glial cyst
Boido M.; Garbossa D.; Vercelli A.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/92574
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