中国组织工程研究

中国组织工程研究 ›› 2010, Vol. 14 ›› Issue (5): 919-922.doi: 10.3969/j.issn.1673-8225.2010.05.039

• 器官移植综述 organ transplantation review • 上一篇    下一篇

SM22α启动子及增强子应用于冠状动脉旁路移植血管防治再狭窄的效应

陈  丽，邓勇志   

  1. 山西医科大学第二医院心胸外科，山西省太原市 030001
  • 出版日期:2010-01-29 发布日期:2010-01-29
  • 通讯作者: 邓勇志，教授，主任医师，硕士生导师，山西医科大学第二医院心胸外科，山西省太原市 030001 dengyongzhi@hotmail.com
  • 作者简介:陈 丽★，女，1984年生，山西省吕梁市人，汉族，山西医科大学在读硕士，主要从事移植血管狭窄的防治研究。 chenli253@163.com
  • 基金资助:

    山西省回国留学人员科研资助项目[2008(10)101]*；山西省留学人员科技活动择优资助项目[晋人函字2008(56)]*。

Application of SM22α promoter and enhancer against angiostenosis following coronary artery bypass grafting

Chen Li, Deng Yong-zhi   

  1. Department of Cardiothoracic Surgery, the Second Teaching Hospital, Shanxi Medical University, Taiyuan  030001, Shanxi Province, China
  • Online:2010-01-29 Published:2010-01-29
  • Contact: Deng Yong-zhi, Professor, Chief physician, Master’s supervisor, Department of Cardiothoracic Surgery, the Second Teaching Hospital, Shanxi Medical University, Taiyuan 030001, Shanxi Province, China dengyongzhi@hotmail.com
  • Supported by:

    Scientific Research Foundation for the Returned Overseas Chinese Scholars in Shanxi Province, No. 2008(10)101*; the Scientific Research Foundation for Excellent Overseas Chinese Students in Shanxi Province, No. 2008 (56)*

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摘要：

背景：大隐静脉是冠状动脉旁路移植术最常用的血管材料，但移植血管新生内膜增生和随后发生的粥样硬化所致的移植血管狭窄严重影响远期疗效。
目的：综合分析移植血管狭窄的病理生理及其机制，平滑肌细胞特异性SM22α启动子、SMHC增强子的构建和应用等。
方法：以SM22α promoter，SMHC enhancer，stenosis，Pi3k，RNAi/RNA interference为检索词，检索PubMed数据库、HighWire数据库和CNKI数据库(1981-01/2009-10)。文献检索语种限制为英文和中文。纳入与移植血管狭窄，血管平滑肌特异性SM22α启动子及其增强子相关的文献。排除综述文献，重复研究类文献。以血管平滑肌细胞的增殖和凋亡，移植血管新生内膜的增生情况，以及移植血管血栓形成的程度为评价指标。
结果与结论：计算机初检得到8 730篇文献，根据纳入排除标准，对SM22α启动子及移植血管狭窄进行分析。冠状动脉旁路移植后新生内膜增生和血栓形成严重影响远期疗效。PI3K-Akt-mTOR信号通路是调节细胞增殖、迁移和生存的关键通路。局部shRNA干扰靶向沉默Pik3cb可下调PI3K信号通路，有效防治移植血管新生内膜增生。采用血管平滑肌细胞特异性SM22α启动子构建靶向大鼠Pik3cb基因的干扰RNA真核表达载体，既可抑制新生内膜增生，又可防治血栓的形成。利用血管平滑肌细胞特异性的SM22α基因，将SM22α启动子/增强子应用于移植血管，为防治移植血管狭窄和血栓形成提供新的思路。

关键词: 新生内膜增生, 血管平滑肌细胞, SM22&alpha, 启动子, 冠状动脉旁路移植, 再狭窄　

Abstract:

BACKGROUND: Great saphenous vein is the most common vascular material in coronary artery bypass grafting, however, the graft neointimal hyperplasia and subsequent atherosclerosis result in angiostegnosis, which affect the long-term efficacy.
OBJECTIVE: To analyze the pathophysiology and mechanism of the angiostenosis, additionally, to construct smooth muscle cell specific SM22α promoter and SMHC enhancer.
METHODS: The database of PubMed, HighWire and CNKI were retrieved with key words of “SM22α promoter, SMHC enhancer, stenosis, Pi3k and RNAi/RNA interference”. The language was confined to English and Chinese. The literatures correlated with angiostenosis, VSMC-specific SM22α promoter and enhancer were selected. The reviews and overlapped researches were excluded. In vascular smooth muscle cell proliferation and apoptosis of graft neointimal hyperplasia, as well as the extent of graft thrombosis were considered as evaluation index.
RESULTS AND CONCLUSION: More than 8 730 literatures were searched by the computer. According to inclusion and exclusion criteria, the SM22α promoter and angiostenosis were analyzed. The neointimal hyperplasia and thrombosis had a strong impact on prospective efficacy after coronary artery bypass grafting. The PI3K-Akt-mTOR pathway was a crucial signal passage which regulated cell proliferation and migration. RNA interference targeting Pik3cb can efficiently suppress the neointimal hyperplasia through down regulating the PI3K-Akt-mTOR pathway. The shRNA eukaryon expression plasmid vectors targeting rat Pik3cb were constructed using VSMC-specific SM22α promoter. On the one hand, it can suppress the neointimal hyperplasia, and on the other, it can prevent the occurrence of thrombosis.SM22α is a specific gene in vascular smooth muscle cell. The studies that applied VSMC-specific SM22α promoter/enhancer to vascular grafting provide a new strategy to prevent angiostenosis and thrombosis.

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