中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (7): 1275-1279.doi: 10.3969/j.issn.1673-8225.2012.07.032

• 骨髓干细胞 bone marrow stem cells • 上一篇    下一篇

心房纤颤模型犬心房组织基质金属蛋白酶9及组织抑制因子1与纤维化的关系***★

李发鹏，甘天翊，姜  涛，毛  婷，张  健，汤宝鹏   

  1. 新疆医科大学第一附属医院心脏中心, 新疆维吾尔自治区乌鲁木齐市  830054
  • 收稿日期:2011-12-02 修回日期:2011-12-30 出版日期:2012-02-12 发布日期:2012-02-12
  • 通讯作者: 汤宝鹏，博士，主任医师，教授，博士生导师，主要从事心血管疾病的诊治。tangbaopeng@hotmail.com
  • 作者简介:李发鹏★，男，1985年生，甘肃省人，汉族，2008年兰州大学毕业，新疆医科大学在读硕士，主要从事心律失常的基础研究与临床治疗。271920898@qq.com

Relationship of matrix metalloproteinases-9 and inhibitory factor-1 in atrium tissue to atrial fibrosis of atrial fibrillation dogs

Li Fa-peng, Gan Tian-yi, Jiang Tao, Mao Ting, Zhang Jian, Tang Bao-peng   

  1. Heart Center, the First Affiliated Hospital of Xinjiang Medical University, Urumqi  830054, Xinjiang Uygur Autonomous Region, China
  • Received:2011-12-02 Revised:2011-12-30 Online:2012-02-12 Published:2012-02-12
  • Contact: Tang Bao-peng, Doctor, Chief physician, Professor, Doctoral supervisor, Heart Center, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, China tangbaopeng@hotmail.com
  • About author:Li Fa-peng★, Studying for master’s degree, Heart Center, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, China 271920898@qq.com
  • Supported by:

     the National Natural Science Foundation of China, No.30860299*; Natural Science Fund of Xinjiang Uygur Autonomous Region, No. 200821143*; 2010 Specialized Research Fund for the Doctoral Program of Higher Education, No. [2010]217 *

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摘要：

背景：基质金属蛋白酶及其组织抑制因子在心房组织中的相互作用及动态平衡与心房纤颤的发生及维持密切相关。
目的：构建持续性心房纤颤犬模型，观察其心房肌组织基质金属蛋白酶9及其组织抑制因子1的基因表达与心房纤颤及心肌纤维化的关系。
方法：采用慢性快速心房起搏诱发持续性心房纤颤犬模型，并设置假手术组。通过Masson三色法染色计算胶原容积分数来评估纤维化程度，左心房心肌基质金属蛋白酶9及组织抑制因子1的mRNA水平表达使用反转录聚合酶联反应检测，其蛋白水平表达通过蛋白质印迹法测定。
结果与结论：与假手术组相比，持续性心房纤颤模型组心房肌纤维化程度明显增高，胶原容积分数明显增加(P < 0.01)，且基质金属蛋白酶9 mRNA及蛋白表达水平明显增加(P < 0.01)，组织抑制因子1的mRNA及蛋白表达水平明显下降        (P < 0.01)。结果证实，心房纤颤心房组织中基质金属蛋白酶9/组织抑制因子1基因表达的调控失衡以及基质金属蛋白酶9活性的增高与组织抑制因子1活性降低可能是影响胶原代谢、促进或抑制心肌纤维化，造成心房纤颤时心房结构重构的分子机制之一。

关键词: 基质金属蛋白酶, 组织抑制因子, 结构重构, 组织构建

Abstract:

BACKGROUND: Interaction and dynamic balance of matrix metalloproteinases and tissue inhibitory factor in atrial is closely related with the occurrence maintenance of atrial fibrillation (AF).
OBJECTIVE: To investigate the matrix metalloproteinase-9 (MMP-9) and tissue inhibitor-1 of metalloproteinase gene expression in atrial and to evaluate the influence of MMP-9 and tissue inhibitor-1 (TIMP-1) expression on AF and fibrosis.
METHODS: The chronic rapid atrial pacing was used to establish the persistent AF dog model and the sham-operated group was seted. Masson three color staining was used to determine the stage of fibrosis, the expression the left atrial MMP-9 mRNA and TIMP-1 mRNA level was detected through reverse transcriptase polymerase chain reaction. The level of protein expression was determined by Western Blot.
RESULTS AND CONCLUSION: Compared with sham-operated group, the degree of fibrosis and collagen volume fraction (CVF) in persistent AF model group was increased obviously (P < 0.01), and the expression of MMP-9 mRNA was increased obviously as well as its protein expression (P < 0.01). The level of TIMP-1 mRNA and protein expression was decreased obviously       (P < 0.01). The imblanced regulation of gene expression betewwn MMP-9 and TIMP-1 of atrial fibrillation, heighten of MMP-9 activity and reduce of TIMP-1 activity may influence collagen metabolism, promoting or inhibiting the myocardial fibrosis, it is one of the molecular mechanism that cause the reconstruction of atrial structure in atrial fibrillation.
 

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