Valsartan Upregulates Kir2.1 in Rats Suffering from Myocardial Infarction via Casein Kinase 2

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• 作者：Xinran Li ; Hesheng Hu ; Ye Wang ; Mei Xue ; Xiaolu Li…
• 关键词：Myocardial infarction ; CK2 ; Kir2.1 ; Valsartan ; Rat
• 刊名：Cardiovascular Drugs and Therapy
• 出版年：2015
• 出版时间：June 2015
• 年：2015
• 卷：29
• 期：3
• 页码：209-218
• 全文大小：1,358 KB
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• 作者单位：Xinran Li (1)
  Hesheng Hu (2)
  Ye Wang (2)
  Mei Xue (2)
  Xiaolu Li (2)
  Wenjuan Cheng (2)
  Yongli Xuan (1)
  Jie Yin (1)
  Na Yang (1)
  Suhua Yan (2)
  
  1. School of Medicine, Shandong University, Ji’nan, Shandong, China
  2. Department of Cardiology, Shandong Provincial Qianfoshan Hospital, No. 16766 Jingshi Road, Jinan, 250014, Shandong Province, China
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Cardiology
  
• 出版者：Springer Netherlands
• ISSN：1573-7241

文摘

Purpose Myocardial infarction (MI) results in an increased susceptibility to ventricular arrhythmias, due in part to decreased inward-rectifier K+ current (IK1), which is mediated primarily by the Kir2.1 protein. The use of renin-angiotensin-aldosterone system antagonists is associated with a reduced incidence of ventricular arrhythmias. Casein kinase 2 (CK2) binds and phosphorylates SP1, a transcription factor of KCNJ2 that encodes Kir2.1. Whether valsartan represses CK2 activation to ameliorate IK1 remodeling following MI remains unclear. Methods Wistar rats suffering from MI received either valsartan or saline for 7?days. The protein levels of CK2 and Kir2.1 were each detected via a Western blot analysis. The mRNA levels of CK2 and Kir2.1 were each examined via quantitative real-time PCR. Results CK2 expression was higher at the infarct border; and was accompanied by a depressed IK1/Kir2.1 protein level. Additionally, CK2 overexpression suppressed KCNJ2/Kir2.1 expression. By contrast, CK2 inhibition enhanced KCNJ2/Kir2.1 expression, establishing that CK2 regulates KCNJ2 expression. Among the rats suffering from MI, valsartan reduced CK2 expression and increased Kir2.1 expression compared with the rats that received saline treatment. In vitro, hypoxia increased CK2 expression and valsartan inhibited CK2 expression. The over-expression of CK2 in cells treated with valsartan abrogated its beneficial effect on KCNJ2/Kir2.1. Conclusions AT1 receptor antagonist valsartan reduces CK2 activation, increases Kir2.1 expression and thereby ameliorates IK1 remodeling after MI in the rat model.