Investigation of Pathogenetic Mechanisms of Spinal Cord Insury using Bcl-2/Bax Transgenic and Knockout Mice

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In this research project, we investigated roles of neuronal cell apoptosis (programmed cell death) secondary to the primary injury in aggravation of traumatic lesion in the spinal cord. For this purpose, we used transgenic/knockout mice of Bcl-2 family genes which are important in regulation of cellular apoptosis. We first established a mouse model of spinal cord injury using a pneumatic impact device and its neurological evaluating system. Applying the model system on Bcl-2 transgenic mice, we obtained the following results:1) Post traumatic neurologic recovery showed a trend to be better in Bcl-2 transgenic mice than in wild-type mice2) Lesion volume assessed by histological quantative evaluation showed a statistically significant difference between wild-type mice (5.1 ± 0.8 x 10^<-2> ml) and Bcl-2 transgenic mice (2.9±0.5x10^<-2> ml).These results indicate that extension of traumatic lesion after a spinal cord injury is largely affected by the-anti- and pro-apoptotic effects of Bcl-2 family proteins. We therefore suggest that Bcl-2 family proteins can be important therapeutic targets in prevention of secondary damage in spinal cord injury.