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.

OBJECTIVES:

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: Li-na Zhao, Lu Fu, Qian-ping Gao, Rong-sheng Xie, Jun-xian Cao
• Journal: The Canadian journal of cardiology (Can J Cardiol) 2011 Nov-Dec Vol. 27 Issue 6 Pg. 826-33 ISSN: 1916-7075 [Electronic] England
• PMID: 21683547 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2011 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.

Chemical References

• Potassium Channels, Tandem Pore Domain
• RNA, Messenger
• potassium channel protein TREK-1

Topics

• Animals
• Disease Models, Animal
• Gene Expression Regulation
• Heart Ventricles (metabolism, pathology)
• Male
• Myocardial Infarction (genetics, metabolism, physiopathology)
• Myocardium (metabolism, pathology)
• Patch-Clamp Techniques
• Potassium Channels, Tandem Pore Domain (biosynthesis, genetics)
• RNA, Messenger (genetics)
• Rats
• Rats, Sprague-Dawley
• Real-Time Polymerase Chain Reaction