title: Stress protein expression in early phase spinal cord ischemia/reperfusion injury.
abstract: Spinal cord ischemia/reperfusion injury is a stress injury to the spinal cord. Our previous studies using differential proteomics identified 21 differentially expressed proteins (n > 2) in rabbits with spinal cord ischemia/reperfusion injury. Of these proteins, stress-related proteins included protein disulfide isomerase A3, stress-induced-phosphoprotein 1 and heat shock cognate protein 70. In this study, we established New Zealand rabbit models of spinal cord ischemia/reperfusion injury by abdominal aorta occlusion. Results demonstrated that hind limb function initially improved after spinal cord ischemia/reperfusion injury, but then deteriorated. The pathological morphology of the spinal cord became aggravated, but lessened 24 hours after reperfusion. However, the numbers of motor neurons and interneurons in the spinal cord gradually decreased. The expression of protein disulfide isomerase A3, stress-induced-phosphoprotein 1 and heat shock cognate protein 70 was induced by ischemia/reperfusion injury. The expression of these proteins increased within 12 hours after reperfusion, and then decreased, reached a minimum at 24 hours, but subsequently increased again to similar levels seen at 6-12 hours, showing a characterization of induction-inhibition-induction. These three proteins were expressed only in cytoplasm but not in the nuclei. Moreover, the expression was higher in interneurons than in motor neurons, and the survival rate of interneurons was greater than that of motor neurons. It is assumed that the expression of stress-related proteins exhibited a protective effect on neurons.
authors.affiliation: Team of Spine and Spinal Cord, Department of Orthopedics, China-Japan Friendship Hospital of Jilin University, Changchun 130033, Jilin Province, China.
authors.forename: Shanyong
authors.initials: S
authors.lastname: Zhang
authors.affiliation: Team of Skeletal Trauma, Department of Orthopedics, the Second Hospital of Jilin University, Changchun 130033, Jilin Province, China.
authors.forename: Dankai
authors.initials: D
authors.lastname: Wu
authors.affiliation: Team of Skeletal Trauma, Department of Orthopedics, the Second Hospital of Jilin University, Changchun 130033, Jilin Province, China.
authors.forename: Jincheng
authors.initials: J
authors.lastname: Wang
authors.affiliation: Team of Spine and Spinal Cord, Department of Orthopedics, China-Japan Friendship Hospital of Jilin University, Changchun 130033, Jilin Province, China.
authors.forename: Yongming
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Team of Spine and Spinal Cord, Department of Orthopedics, China-Japan Friendship Hospital of Jilin University, Changchun 130033, Jilin Province, China.
authors.forename: Guoxiang
authors.initials: G
authors.lastname: Wang
authors.affiliation: Team of Spine and Spinal Cord, Department of Orthopedics, China-Japan Friendship Hospital of Jilin University, Changchun 130033, Jilin Province, China.
authors.forename: Maoguang
authors.initials: M
authors.lastname: Yang
authors.affiliation: Team of Spine and Spinal Cord, Department of Orthopedics, China-Japan Friendship Hospital of Jilin University, Changchun 130033, Jilin Province, China.
authors.forename: Xiaoyu
authors.initials: X
authors.lastname: Yang
keywords: apoptosis; grants-supported paper; heat shock cognate protein 70; necrosis; neural regeneration; neuron; neuroregeneration; protein disulfide isomerase A3; spinal cord ischemia/reperfusion injury; stress-induced-phosphoprotein 1