Lou J, Lenke L G, Xu F, O'Brien M
Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, Missouri, USA.
Spine (Phila Pa 1976). 1998 Mar 1;23(5):517-23. doi: 10.1097/00007632-199803010-00001.
An acute mechanical rat spinal cord injury model was used to investigate in vivo Bcl-2 oncogene overexpression in neuronal tissue.
To introduce the Bcl-2 oncogene in vivo by a recombinant adenovirus vector into rat spinal cord tissue, and to investigate any potential protective effect on neural tissue in the zone of injury in a rat spinal cord model.
The Bcl-2 oncogene inhibits apoptotic and necrotic neural cell death in vitro by regulating an antioxidant pathway at sites of free radical generation. Thus, overexpression of the Bcl-2 oncogene may have a role in limiting the secondary injury cascade of spinal cord injury through its regulation of antioxidants.
After confirmation of Bcl-2 gene expression in vitro and in vivo in the rat spinal cord, a weight-drop spinal cord injury model was performed on seven rats with prior Bcl-2 inoculation, and on seven rats with prior B-gal inoculation (controls).
In vivo Bcl-2 expression was documented by immunostaining. After spinal cord harvest, quantification of percentage preserved tissue at the spinal cord injury site suggested that Bcl-2 overexpression confers neuroprotection.
In vivo Bcl-2 oncogene overexpression was successfully induced in neuronal tissue. After Bcl-2 oncogene expression in the rat spinal cord, the zone of microscopic injury was diminished. Further investigation of the Bcl-2 oncogene for potentially enhancing neuronal survival after spinal cord injury appears indicated.
