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Updated: Jun 24, 2026
A Neurosphere Assay to Evaluate Endogenous Neural Stem Cell Activation in a Mouse Model of Minimal Spinal Cord Injury
Published on: September 13, 2018
High-dose corticosteroids after spinal cord injury reduce neural progenitor cell proliferation
A Schröter1, R M Lustenberger, F J Obermair
1Brain Research Institute, University of Zurich, Zurich, Switzerland.
Abstract:
We assessed whether a clinical dose of the anti-inflammatory drug methylprednisolone (MP) given to adult mice acutely after spinal cord injury (SCI) influences spinal cord or hippocampal progenitor cells. Mice underwent a thoracic dorsal hemisection of the spinal cord and received 30 mg/kg MP immediately and 24 h post-lesion. 5-Bromo-2-deoxyuridine (BrdU) was administered after lesion either acutely (1-6 days) or late (22-27 days) to label proliferating cells. Reaction of microglia/macrophages was quantified 7 days post-lesion and proliferation as well as differentiation of neural progenitor cells (NPCs) was analyzed after two survival times (7 days and 28 days). We also tested the influence of MP on microglia and adult NPCs in vitro. MP treatment reduced the number of cells proliferating acutely after SCI in the spinal cord and hippocampus. Besides reducing activation and proliferation of microglia/macrophages in the spinal cord, MP also decreased the number of oligodendrocyte progenitor cells (OPCs). Analysis of acutely BrdU-labeled cells at 28 days post-lesion suggests that proliferation and number of OPCs were changed chronically. Late proliferating cells were no longer influenced by the glucocorticoid regimen. In vitro experiments showed an inhibitory effect of MP on adult spinal cord and hippocampal progenitor cell proliferation. Both cell types express the glucocorticoid and mineralocorticoid receptors allowing a direct effect of MP. Our results show that MP reduces OPC proliferation after SCI either by affecting progenitor cells directly or via its anti-inflammatory effects. These findings open the question to which extent MP treatment limits the repair capacity of endogenous progenitor cells after CNS injury.
Insights
Methylprednisolone (MP) treatment after spinal cord injury (SCI) reduces progenitor cell proliferation in the spinal cord and hippocampus. This anti-inflammatory drug may limit the central nervous system
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- Spinal cord injury (SCI) triggers inflammatory responses and affects neural progenitor cells (NPCs).
- Methylprednisolone (MP), a potent anti-inflammatory drug, is used clinically after SCI.
- The impact of MP on endogenous progenitor cells post-SCI remains incompletely understood.
Purpose of the Study:
- To investigate the effect of a clinical dose of MP on spinal cord and hippocampal progenitor cells following acute SCI in adult mice.
- To determine if MP influences microglia/macrophage activation and NPC proliferation and differentiation.
- To explore the direct effects of MP on progenitor cells in vitro.
Main Methods:
- Adult mice received MP (30 mg/kg) immediately and 24 hours after thoracic dorsal hemisection SCI.
- Cell proliferation was assessed using 5-Bromo-2-deoxyuridine (BrdU) labeling at acute (1-6 days) and late (22-27 days) time points.
- Microglia/macrophage reaction, NPC proliferation, and differentiation were analyzed at 7 and 28 days post-lesion.
- In vitro experiments tested MP's effect on adult spinal cord and hippocampal progenitor cells.
Main Results:
- MP treatment reduced acute cell proliferation in the spinal cord and hippocampus post-SCI.
- MP decreased microglia/macrophage activation and proliferation, and reduced oligodendrocyte progenitor cell (OPC) numbers.
- Chronic effects indicated altered OPC proliferation and numbers, while late proliferating cells were unaffected.
- In vitro studies demonstrated MP's inhibitory effect on progenitor cell proliferation, mediated by glucocorticoid and mineralocorticoid receptors.
Conclusions:
- MP reduces OPC proliferation after SCI, potentially through direct effects on progenitor cells or via anti-inflammatory actions.
- The findings raise concerns about MP's potential to limit endogenous repair capacity following central nervous system injury.
- Further research is needed to elucidate the long-term consequences of MP treatment on neural repair mechanisms.
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