文章摘要
杨成伟,刘 锋,殷国勇,张 宁,胡志毅,蔡卫华,任永信.GIT1和ERK1/2在兔脊髓缺血再灌注损伤中作用的初步研究[J].南京医科大学学报,2008,28(4):508~512
GIT1和ERK1/2在兔脊髓缺血再灌注损伤中作用的初步研究
The role of GIT1 and ERK1/2 in reperfusion of ischemic spinal cord
投稿时间:2007-11-04  
DOI:10.7655
中文关键词: 脊髓缺血再灌注  GIT1  ERK1/2  细胞凋亡
英文关键词: reperfusion of ischemic spinal cord  GIT1  ERK1/2  apoptosis
基金项目:国家自然科学基金(30670867);江苏省自然科学基金(BK2006249)
作者单位
杨成伟 南京医科大学第一附属医院骨科江苏 南京 210029 
刘 锋  
殷国勇  
张 宁  
胡志毅  
蔡卫华  
任永信  
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中文摘要:
      目的:研究G蛋白耦联受体激酶相互作用分子1(G-protein-coupled receptor kinase interacting protein 1,GIT1),细胞外信号调节激酶1/2(Extracellular signal-regulated kinases 1 and 2,ERK1/2)在脊髓缺血再灌注损伤过程中的作用。方法:电镜观察缺血30 min再灌注不同时间段[A组(对照组)再灌注0 min、B组 再灌注30 min、C组 再灌注2 h、D组 再灌注8 h]脊髓组织标本的形态学改变,Western blot 检测各组脊髓标本中ERK1/2 和GIT1 的表达及其磷酸化,免疫共沉淀分析GIT1同活化的ERK1/2(phospho-ERK1/2,pERK1/2)相互作用的变化,免疫组织化学分析pERK1 /2在神经细胞内的定位表达。结果:电镜结果显示D组脊髓神经细胞出现早期凋亡的征象;Western blot结果显示pERK1/2的表达、GIT1的磷酸化在C、D二组较对照组明显增加且均随再灌注时间延长呈明显增加的趋势;免疫共沉淀结果显示GIT1-pERK1/2结合力在C、 D两组较对照组明显增加;免疫组织化学结果显示pERK1/2明显滞留于C、D两组的脊髓神经细胞胞浆区内。结论:缺血再灌注损伤过程中ERK1/2的活化以及在胞核外区域的滞留可能导致了脊髓神经细胞的凋亡,而GIT1作为细胞浆内局部黏附蛋白同pERK1/2的结合可能导致了其在胞浆区的滞留。
英文摘要:
       Objective:To investigate the role and mechanism of G-protein-coupled receptor kinase interacting protein 1(GIT1) and Extracellular signal-regulated kinases 1 and 2(ERK1/2) in reperfusion of ischemic spinal cord. Methods:The morphology of spinal cord was observed by electron microscope in different time courses after ischemia/reperfusion injury[group A(control group),group B(ischemia 30 min/reperfusion 30 min),group C(ischemia 30 min/reperfusion 2 h),group D(ischemia 30 min/reperfusion 8 h)]. The phosphorylation of ERK1/2 and GIT1 was detected by Western blot. The interaction between GIT1 and pERK1/2 was detected by coimmunoprecipitation. The localization of pERK1/2 was analyzed by immunohistochemistry. Results:The apoptosis of neurocytes of spinal cord undergoing ischemia/reperfusion injury in group D was detected by electronmicroscope. The phosphorylation of ERK1/2 and GIT1 and the interaction between GIT1 and pERK1/2 significantly increased in group C and D. Immunohistochemistry results showed that the stagnation of pERK1/2 was observed in the cytoplasma of neurocytes in group C and D. Conclusion:The stagnation of pERK1/2 in the cytoplasm might act as apoptosis signals contributing to the apoptosis of neurocytes of spinal cord after ischemia/reperfusion injury,and the interaction between GIT1 and pERK1/2 might cause the stagnation of pERK1/2 in the cytoplasm of neurocytes.
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