title: miR-539 as a key negative regulator of the MEK pathway in myocardial infarction.
abstract: BACKGROUND
  Myocardial infarction is one of the most common causes of death, and the number of individuals at risk is increasing. A rapid and accurate differential diagnosis of myocardial infarction is crucial for timely interventions and for improvement of the prognosis. However, it is difficult to achieve using current methods. To better manage this condition, improved tools for risk prediction, including more accurate biomarkers, are needed.
  
  
  METHODS
  We studied the expression of microRNA-539 (miR-539) and of MEK protein using a rat model of myocardial infarction.
  
  
  RESULTS
  The results of our experiments demonstrated an increase in the expression of miR-539 and a decrease in the expression of MEK. Furthermore, we observed that miR-539 inhibited the expression of MEK through targeting of the 3'UTR of MEK; this led not only to suppressed proliferation but also to apoptosis and autophagy of H9C2 cells.
  
  
  CONCLUSIONS
  Overexpression of miR-539 plays a role in the degree of myocardial infarction. On the basis of our results, we conclude that miR-539 may be a potential therapeutic target for myocardial infarction.
authors.affiliation: Department of Cardiovascular Surgery, The General Hospital of Shenyang Military Region, No. 83Wenhua Road, 110016, Shenhe District, Shenyang, Liaoning, China.
authors.forename: J
authors.initials: J
authors.lastname: Hui
authors.affiliation: Department of Cardiovascular Surgery, The General Hospital of Shenyang Military Region, No. 83Wenhua Road, 110016, Shenhe District, Shenyang, Liaoning, China. wanghuishan2016@sina.com.
authors.forename: W
authors.initials: W
authors.lastname: Huishan
authors.affiliation: Department of Cardiovascular Surgery, The General Hospital of Shenyang Military Region, No. 83Wenhua Road, 110016, Shenhe District, Shenyang, Liaoning, China.
authors.forename: L
authors.initials: L
authors.lastname: Tao
authors.affiliation: Department of Cardiovascular Surgery, The General Hospital of Shenyang Military Region, No. 83Wenhua Road, 110016, Shenhe District, Shenyang, Liaoning, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Zhonglu
authors.affiliation: Department of Cardiovascular Surgery, The General Hospital of Shenyang Military Region, No. 83Wenhua Road, 110016, Shenhe District, Shenyang, Liaoning, China.
authors.forename: Z
authors.initials: Z
authors.lastname: Renteng
authors.affiliation: Department of Cardiovascular Surgery, The General Hospital of Shenyang Military Region, No. 83Wenhua Road, 110016, Shenhe District, Shenyang, Liaoning, China.
authors.forename: H
authors.initials: H
authors.lastname: Hongguang
mesh_terms: D020413:3' Untranslated Regions / Q000235:genetics; D000818:Animals; D017209:Apoptosis / Q000235:genetics; D001343:Autophagy / Q000235:genetics; D016923:Cell Death / Q000235:genetics; D002460:Cell Line; D049109:Cell Proliferation / Q000235:genetics; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006801:Humans; D020935:MAP Kinase Signaling System / Q000235:genetics*; D035683:MicroRNAs / Q000235:genetics*; D009203:Myocardial Infarction / Q000235:genetics*; D017207:Rats, Sprague-Dawley; D018570:Risk Assessment
chemical_list: D020413:3' Untranslated Regions; C000612890:MIRN539 microRNA, rat; D035683:MicroRNAs
keywords: Apoptosis; Autophagic cell death; Cellular proliferation; MEKs; Myocardial infarction