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Updated: Aug 18, 2026
A Contusion Model of Severe Spinal Cord Injury in Rats
Published on: August 17, 2013
Prolonged lesional expression of RhoA and RhoB following spinal cord injury
Sabine Conrad1, Hermann J Schluesener, Katrin Trautmann
1Institute of Brain Research, D-72076 Tuebingen, Germany.
Abstract:
Inhibition of the small GTPase ras homology protein (Rho) or its downstream target, the Rho-associated kinase (ROCK), has been shown to promote axon regeneration and to improve functional recovery following spinal cord injury (SCI) in the adult rat. Here, we have analyzed the expression of RhoA and RhoB following spinal cord injury in order to assess whether Rho is a possible target for late pharmacological intervention. In control spinal cords, RhoA(+) cells were almost absent, whereas RhoB was localized to some ependymal cells, a few microglia, and some dissociated neurons. In injured spinal cords, RhoA(+) and RhoB(+)cells accumulated at perilesional areas and in the developing necrotic core early after injury at day 1. After reaching their maximum levels (RhoA at day 3; RhoB at day 1), RhoA(+) and RhoB(+) cell numbers remained significantly elevated until day 28. In areas remote from the lesion (> or =0.75 mm), a more discrete accumulation of RhoA(+) and RhoB(+) cells was observed, primarily in areas of ongoing Wallerian degeneration. RhoA and RhoB were predominantly expressed by polymorphonuclear granulocytes, ED1(+) microglia/macrophages, oligodendrocytes, some neurons, and swollen axons/neurites. Furthermore, expression was located to lesional, reactive astrocytes and fibroblastoid cells confined to areas of scar formation. Our experiments have determined that most RhoA(+) and RhoB(+) cells (>70%) are of mononuclear origin. The persistent presence of lesional RhoA(+) and RhoB(+) axon/neurite fibers over a period of 4 weeks after injury suggests that Rho inhibition is a putative therapeutic concept also for delayed intervention after SCI.
Insights
Inhibition of the small GTPase ras homology protein (Rho) and its target Rho-associated kinase (ROCK) aids axon regeneration after spinal cord injury (SCI). This study shows RhoA and RhoB persist post-injury, suggesting Rho inhibition is viable for delayed SCI treatment.
Area of Science:
- Neuroscience
- Regenerative Medicine
- Pharmacology
Background:
- Inhibition of the small GTPase ras homology protein (Rho) or its downstream target, Rho-associated kinase (ROCK), promotes axon regeneration and functional recovery after spinal cord injury (SCI).
- The expression patterns of RhoA and RhoB following SCI are not fully understood, particularly concerning their potential as targets for late-stage pharmacological intervention.
Purpose of the Study:
- To analyze the expression of RhoA and RhoB in the spinal cord following injury.
- To assess the potential of Rho inhibition as a therapeutic strategy for delayed intervention in SCI.
Main Methods:
- Immunohistochemical analysis of RhoA and RhoB expression in control and injured rat spinal cords at various time points post-injury (days 1-28).
- Identification of cell types expressing RhoA and RhoB, including microglia/macrophages, oligodendrocytes, neurons, astrocytes, and fibroblastoid cells.
- Assessment of RhoA and RhoB expression in areas remote from the lesion and in Wallerian degeneration zones.
Main Results:
- RhoA(+) and RhoB(+) cells significantly accumulated in perilesional areas and the necrotic core early after SCI, remaining elevated for at least 28 days.
- RhoA and RhoB were expressed by various cell types, including inflammatory cells, glial cells, neurons, and reactive astrocytes.
- Persistent expression of RhoA and RhoB was observed in axon/neurite fibers for up to 4 weeks post-injury.
Conclusions:
- RhoA and RhoB are persistently expressed in the injured spinal cord, involving multiple cell types and persisting axon/neurite fibers.
- The sustained presence of RhoA and RhoB suggests that Rho inhibition remains a viable therapeutic concept for delayed intervention after SCI.
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