Stress injuries to the spinal cord cause protein expression, which could be valuable in developing injury control measures, according to a new study in animals
Spinal cord ischemia/reperfusion injury is a stress injury to the spinal cord. Therefore, research on the expression of stress-related proteins in neurons could be of great significance for the pathological mechanism and control measures for spinal cord ischemia/reperfusion injury.
Previous studies from Dr Shanyong Zhang and colleagues from China-Japan Friendship Hospital of Jilin University identified 21 differentially expressed proteins in rabbits with spinal cord ischemia/reperfusion injury using differential proteomics.
Of these proteins, stress-related proteins included protein disulfide isomerase A3, stress-induced-phosphoprotein 1 and heat shock cognate protein 70. Their recent study established New Zealand rabbit models of spinal cord ischemia/reperfusion injury by abdominal aorta occlusion. The researchers found that the expression of protein disulfide isomerase A3, stress-induced-phosphoprotein 1 and heat shock cognate protein 70 was induced by ischemia/reperfusion injury, showing a characterisation of induction-inhibition-induction.
These three proteins were expressed only in cytoplasm but not in the nuclei, suggesting that the expression of stress-related proteins exhibited a protective effect on neurons. After spinal cord ischemia/reperfusion injury, heat shock cognate protein 70 expression was detectable in glial cell nuclei in the gray matter and in Schwann cell nuclei in the white matter, possibly because heat shock cognate protein 70 was transported back into nuclei. These findings were published in Neural Regeneration Research.