中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (24): 2225-2235.doi: 10.3969/j.issn.1673-5374.2013.24.002

• 原著:脊髓损伤修复保护与再生 • 上一篇    下一篇

脊髓缺血再灌注损伤早期应激类蛋白的表达变化

  

  • 收稿日期:2013-03-27 修回日期:2013-07-17 出版日期:2013-08-25 发布日期:2013-08-25

Stress protein expression in early phase spinal cord ischemia/reperfusion injury

Shanyong Zhang1, Dankai Wu2, Jincheng Wang2, Yongming Wang1, Guoxiang Wang1, Maoguang Yang1, Xiaoyu Yang1   

  1. 1 Team of Spine and Spinal Cord, Department of Orthopedics, China-Japan Friendship Hospital of Jilin University, Changchun 130033, Jilin Province, China
    2 Team of Skeletal Trauma, Department of Orthopedics, the Second Hospital of Jilin University, Changchun 130033, Jilin Province, China
  • Received:2013-03-27 Revised:2013-07-17 Online:2013-08-25 Published:2013-08-25
  • Contact: Xiaoyu Yang, Ph.D., Professor, Team of Spine and Spinal Cord, Department of Orthopedics, China-Japan Friendship Hospital of Jilin University, Changchun 130033, Jilin Province, China, yangxiaoyu88@ sina.com.
  • About author:Shanyong Zhang, Studying for doctorate, Attending physician. Shanyong Zhang and Dankai Wu contributed equally to this article.
  • Supported by:

    国家自然科学基金（30872609）

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摘要：

脊髓缺血再灌注损伤对脊髓是一种应激性损害，细胞中存在应激蛋白质能够抵御不良应激损害。作者所在课题组前期利用差异蛋白质组学研究方法鉴定出兔脊髓缺血再灌注损伤中2倍以上差异表达蛋白21个，其中应激相关蛋白为蛋白质二硫键异构酶3、磷酸化应激诱导蛋白和热激活蛋白70识别蛋白三种。实验以夹闭腹主动脉的方式建立新西兰白兔脊髓缺血再灌注损伤模型，发现兔脊髓缺血再灌注损伤后后肢功能好转后恶化，脊髓病理形态损害逐渐加重，再灌注24h后减轻，而脊髓中运动神经元及中间神经元数量逐渐减少，脊髓中蛋白质二硫键异构酶3、磷酸化应激诱导蛋白、热激活蛋白70识别蛋白三种蛋白都可被缺血再灌注损伤诱导表达，再灌注后12h内表达增高，随后表达降低，至再灌注24h表达降低至最低点，而后表达又恢复至再灌注后6-12h水平，表现出诱导-抑制-再次诱导的特点。3种蛋白只在神经元的胞浆中表达，未见胞核表达，且在中间神经元胞浆表达量多于运动神经元，而中间神经元存活率高于运动神经元，推测应激相关蛋白表达对神经元有保护作用。

关键词: 神经再生, 脊髓损伤, 脊髓, 缺血再灌注损伤, 蛋白质二硫键异构酶A3, 磷酸化应激诱导蛋白, 热激活蛋白70识别蛋白, 神经元, 坏死, 凋亡, 基金资助文章

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-induc- tion. 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.

Key words: neural regeneration, spinal cord ischemia/reperfusion injury, protein disulfide isomerase A3, stress-induced-phosphoprotein 1, heat shock cognate protein 70, neuron, necrosis, apoptosis, grants-supported paper, neuroregeneration