Related Experiment Video
Updated: Jul 28, 2026
Neural Stem Cell Transplantation in Experimental Contusive Model of Spinal Cord Injury
Published on: December 17, 2014
Role of the bcl-2 gene after contusive spinal cord injury in mice
Toshitaka Seki1, Kazutoshi Hida, Mitsuhiro Tada
1Department of Neurosurgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan. toseki@med.hokudai.ac.jp
Objective:
Apoptosis is indicated to have an important role in the secondary injury mechanisms of acute spinal cord injury (SCI). The proto-oncogene bcl-2 has been demonstrated to prevent apoptotic cell death in a wide variety of cell types. This study examined the recovery of behavioral function and histopathological variables after controlled-impact SCI in human bcl-2 transgenic (TG) mice and control mice.
Methods:
Six bcl-2 TG mice and five control mice were subjected to controlled-impact SCI of moderate severity at T10, with the use of a pneumatic impact device (0.25-mm-deep deformation; impact velocity, 2 m/s). Functional deficits were evaluated at times up to 28 days after SCI, with assessments of hindlimb reflexes and coordinated motor function. The extents of the lesions were histopathologically analyzed and quantified with morphometric measurements.
Results:
Both control and bcl-2 TG mice exhibited profound deficits immediately after injury, with subsequent gradual symptomatic recovery. The mean functional scores for the control mice were lower than those for the bcl-2 TG mice, although the Mann-Whitney U test revealed no significant differences. The mean lesion volume for the bcl-2 TG mice (mean +/- standard deviation, 2.9 +/- 1.1 x 10(-2) mm(3)) was significantly lower than that for the control mice (5.1 +/- 0.8 x 10(-2) mm(3); unpaired t test, P = 0.0101). Immunohistological analysis of the spinal cords from the bcl-2 TG mice revealed marked expression of Bcl-2 at the injury site and in adjacent regions.
Conclusion:
Our results suggest that overexpression of the bcl-2 gene may play a protective role in neuropathological sequelae after SCI.
Insights
Overexpression of the bcl-2 gene in mice after spinal cord injury (SCI) reduced lesion volume. This suggests bcl-2 may protect against secondary injury mechanisms in SCI.
Area of Science:
- Neuroscience
- Molecular Biology
- Regenerative Medicine
Background:
- Apoptosis plays a key role in secondary injury after acute spinal cord injury (SCI).
- The proto-oncogene bcl-2 inhibits apoptosis in various cell types.
- Understanding bcl-2's role in SCI is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the effect of bcl-2 gene overexpression on functional recovery and histopathology after controlled-impact SCI in mice.
- To assess the protective potential of bcl-2 in SCI models.
Main Methods:
- Controlled-impact SCI was induced in bcl-2 transgenic (TG) and control mice.
- Behavioral function (hindlimb reflexes, motor coordination) was assessed up to 28 days post-injury.
- Lesion volume was quantified using morphometric analysis; Bcl-2 expression was analyzed via immunohistology.
Main Results:
- Both groups showed initial deficits with gradual recovery; bcl-2 TG mice had lower mean functional scores, though not statistically significant.
- Mean lesion volume was significantly smaller in bcl-2 TG mice (2.9 x 10(-2) mm(3)) compared to controls (5.1 x 10(-2) mm(3)).
- Marked Bcl-2 expression was observed in the injury site and surrounding areas of bcl-2 TG mice.
Conclusions:
- Overexpression of the bcl-2 gene demonstrates a protective effect in the neuropathological sequelae following SCI.
- Targeting bcl-2 may represent a promising therapeutic avenue for mitigating secondary damage after spinal cord injury.
