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Neural Stem Cell Transplantation in Experimental Contusive Model of Spinal Cord Injury
Published on: December 17, 2014
Phenotypic changes in NG2+ cells after spinal cord injury
Judith M Lytle1, Stefano Vicini, Jean R Wrathall
1Interdisciplinary Program in Neuroscience, Georgetown University Medical Center, Washington, DC, USA.
Spinal cord injury (SCI) causes significant oligodendrocyte loss. Adult NG2(+) cells differ from postnatal ones and change after SCI, impacting repair potential.
Area of Science:
- Neuroscience
- Cell Biology
- Regenerative Medicine
Background:
- Spinal cord injury (SCI) leads to rapid oligodendrocyte loss.
- NG2-expressing cells proliferate post-SCI and may replenish lost oligodendrocytes and astrocytes.
- Understanding adult NG2(+) cell characteristics is crucial for SCI repair strategies.
Purpose of the Study:
- To compare NG2(+) cells from adult injured spinal cords with those from uninjured adult and early postnatal cords.
- To investigate the antigenic and physiological properties of NG2(+) cells after SCI.
- To assess the potential of NG2(+) cells to differentiate into mature oligodendrocytes post-injury.
Main Methods:
- Isolation and dissociation of NG2(+) cells from adult injured and uninjured, and early postnatal spinal cords.
- Immunocytochemistry for NG2, nestin, A2B5, O4, and O1 markers.
- Patch clamp analysis to evaluate voltage-gated potassium currents.
- Assessment of cellular response to GABA and glutamate.
Main Results:
- More NG2(+) cells were isolated from injured cords, but microglia/macrophages predominated.
- Adult NG2(+) cells showed distinct antigenic profiles (NG2+/A2B5-) compared to postnatal cells (NG2-/A2B5+).
- NG2(+) cells from injured adults exhibited altered potassium currents and reduced responsiveness to GABA/glutamate versus postnatal cells.
Conclusions:
- Adult NG2(+) cells are antigenically and physiologically distinct from early postnatal NG2(+) cells.
- Contusive SCI induces significant changes in adult NG2(+) cell properties.
- These alterations may affect the capacity of NG2(+) cells to contribute to spinal cord repair after injury.
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