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Updated: May 2, 2026
Direct Injection of a Lentiviral Vector Highlights Multiple Motor Pathways in the Rat Spinal Cord
Published on: March 15, 2019
Effect of lentivirus-mediated RNA interference of APC-Cdh1 expression on spinal cord injury in rats
1Department of Anesthesiology, Tongji Hospital, Tongi Medical College, Huazhong University of Science and Technology, Wuhan, China.
Abstract:
This study investigated cadherin-1 (Cdh1) expression in the sensorimotor cortex of rats after spinal cord injury (SCI). The repairing effect of Cdh1 was evaluated by silencing its expression with lentivirus-mediated RNAi. Twenty male Sprague-Dawley (SD) rats were randomly divided into a normal group and an operation group. Rats of the operation group were given SCI by the Allen method (T10-T11). Cdh1 expression in the sensorimotor cortex was examined by quantitative real-time polymerase chain reaction (PCR) and Western blot analysis. Thirty male SD rats were divided into a sham-operation (SO) group, a lentivirus vector (LV) group, and a recombinant lentivirus (RL) group. Rat behavior was evaluated using the Basso-Beattie-Bresnahan (BBB) test every week. Ten days after injection, Cdh1 expression was examined by quantitative real-time PCR and Western blot. Six weeks after injury, animals were injected with biotinylated dextran amine-Texas Red (BDA-TR), and then at 8 weeks, spinal cords were removed and sectioned in serial order. The expression of Cdh1 mRNA was significantly higher in the operation than in the normal group (P < 0.05). The expression of Cdh1 mRNA was lower in the RL than in the SO or LV groups at 10 days after injection (P < 0.05). In addition, the BBB score was higher for the RL than for the SO or LV groups at 6 weeks after injury (P < 0.05). A novel population of BDA-labeled axons was observed extending past the lesion in the RL group, which was rarely observed in the SO and LV groups. These results suggest that the anaphase-promoting complex-Cdh1 may play an important role in inhibiting axonal growth.
Insights
Spinal cord injury (SCI) increases cadherin-1 (Cdh1) expression, which inhibits axonal regrowth. Silencing Cdh1 promotes functional recovery and axonal regeneration after SCI in rats.
Area of Science:
- Neuroscience
- Molecular Biology
- Regenerative Medicine
Background:
- Spinal cord injury (SCI) often leads to permanent neurological deficits.
- Cadherin-1 (Cdh1) is implicated in cellular processes, but its role in axonal regeneration after SCI is unclear.
Purpose of the Study:
- To investigate the role of Cdh1 in the sensorimotor cortex following SCI.
- To evaluate the therapeutic potential of targeting Cdh1 for axonal regeneration and functional recovery.
Main Methods:
- Spinal cord injury model in Sprague-Dawley rats.
- Quantitative real-time PCR and Western blot to assess Cdh1 expression.
- Lentivirus-mediated RNA interference (RNAi) to silence Cdh1.
- Basso-Beattie-Bresnahan (BBB) behavioral testing.
- Biotinylated dextran amine (BDA) tracing to visualize axonal growth.
Main Results:
- Cdh1 mRNA expression was significantly upregulated in the sensorimotor cortex after SCI.
- Silencing Cdh1 using recombinant lentivirus (RL) reduced Cdh1 expression.
- RL treatment led to improved BBB scores, indicating enhanced motor function.
- BDA tracing revealed increased axonal regeneration past the lesion site in the RL group.
Conclusions:
- Anaphase-promoting complex-Cdh1 plays an inhibitory role in axonal regeneration after SCI.
- Targeting Cdh1 presents a potential therapeutic strategy for promoting recovery and axonal growth post-injury.
