江苏省科技期刊可视化阅读平台

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江苏科技信息 ›› 2016, Vol. 33 ›› Issue (30): 79-80.doi: 10.3969/j.issn.1004-7530.2016.30.018

• 论文 • 上一篇    

心衰大鼠心肌细胞过表达β2受体对SERCA2a/PLB的影响及分子机制研究

吕茜, 刘颖, 王雷, 王洁, 宫海滨   

  1. 徐州市心血管病研究所，江苏徐州 221009; 徐州市中心医院，江苏徐州 221009
  • 出版日期:2016-10-25 发布日期:2016-10-25
  • 基金资助:
    市科技局社会发展项目%项目编号XM13B043。徐州市社会发展项目%项目编号XM12B062。江苏省临床医学科技专项%项目编号BL2012019。

Effect of overexpression of β2 receptor on SERCA2a/PLB and its molecular mechanism in cardiac muscle cells of rats with heart failure

Lyu Qian, Liu Ying, Wang Lei, Wang Jie, Gong Haibing   

  • Online:2016-10-25 Published:2016-10-25

摘要： 目的：检测过表达β2-AR蛋白的慢性心衰大鼠心肌细胞SERCA2a/PLB的改变及相关信号转导通路的改变，初步探讨过表达β2-AR基因影响心衰大鼠心肌细胞收缩功能的分子机制。方法：通过腹主动脉缩窄术建立大鼠慢性心力衰竭模型并采用胶原酶消化法分离心衰大鼠心肌细胞，转染携带β2-AR目的基因的重组腺病毒，通过免疫印迹方法检测β2-AR的过表达对心衰时SERCA2a/PLB的影响，及其导致的心肌收缩功能的改变，探讨过表达β2-AR保护心衰大鼠心肌细胞的分子信号机制。结果：心衰后β2-AR的过表达改善了PLB与SERCA2a的结合与解离，从而调节了SERCA2a对Ca2+的摄取（P<0.05）。结论：心衰大鼠心肌细胞过表达β2-AR后，增加的β2-AR通过PLB/SERCA2a调节了心肌细胞的收缩舒张功能。

关键词: 心力衰竭, β2肾上腺素能受体, 心肌肌浆网Ca2+-ATP酶2a, 受磷蛋白

Abstract: Objective: To detect the changes of SERCA2a/PLB and related signal transduction pathway of myocardial cells in rats with chronic heart failure by expressing β2-AR protein, explore the molecular mechanism of β2-AR gene over expression affect myocardial contractile function in rats with heart failure. Methods: The rat model of chronic heart failure was established by partially banding abdominal aorta and the cadiocyte was isolated with collagenase II, then the cadiocyte was transfected with Adv. β2-AR to observe the change of the key proteins during the myocardial contraction in Western Blot. Results: Overexpressed β2-AR protein modulated the expression of SERCA2a/PLB, and the congsistence of Ca2+ (P<0.05). Conclusions:The overexpressed β2-AR protein can make the cadiocyte antagonist the toxic actioni of heart failure throught the SERCA2a/PLB.