title: Regional differential expression of TREK-1 at left ventricle in myocardial infarction.
abstract: BACKGROUND
  Altered membrane electrophysiology contributes to arrhythmias after myocardial infarction (MI). TREK-1 channel is essential in various physiological and pathological conditions through its regulation on resting membrane potential and voltage-dependent action potential duration.
  
  
  OBJECTIVE
  The aim of this study was to investigate changes in gene expression and electrophysiology of TREK-1 in the left ventricle in a MI model.
  
  
  METHODS
  Fifty-five rats were divided into 5 groups: sham-operated group, 6 hours, 24 hours, 3 days, and 7 days post MI group (n=11 per group). TREK-1 messenger RNA (mRNA) expression level in the infarct region (IR) and infarct border region (IBR) were quantified by real-time polymerase chain reaction (PCR), and TREK-1 current density at the IBR was recorded with whole-cell patch-clamp technique.
  
  
  RESULTS
  TREK-1 mRNA expression decreased significantly in both endocardial and epicardial cells in the infarct region after MI. Conversely, TREK-1 increased significantly in endocardial and epicardial cells from the IBR (P<0.01). Current density of TREK-1 at IBR increased significantly in both epicardial and endocardial cells after MI (P<0.01).
  
  
  CONCLUSIONS
  TREK-1 demonstrates specific changes in expression and electrophysiological function in left ventricle post MI. These results suggest that TREK-1 may participate in pathophysiologic alteration and electrical remodelling of left ventricular myocardium after MI, which may eventually lead to post-MI ventricular arrhythmias.
authors.affiliation: Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
authors.forename: Li-na
authors.initials: LN
authors.lastname: Zhao
authors.forename: Lu
authors.initials: L
authors.lastname: Fu
authors.forename: Qian-ping
authors.initials: QP
authors.lastname: Gao
authors.forename: Rong-sheng
authors.initials: RS
authors.lastname: Xie
authors.forename: Jun-xian
authors.initials: JX
authors.lastname: Cao
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D006352:Heart Ventricles / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009203:Myocardial Infarction / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018408:Patch-Clamp Techniques; D024683:Potassium Channels, Tandem Pore Domain / Q000096:biosynthesis / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics*; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction
chemical_list: D024683:Potassium Channels, Tandem Pore Domain; D012333:RNA, Messenger; C103742:potassium channel protein TREK-1