RGD Reference Report - Regional differential expression of TREK-1 at left ventricle in myocardial infarction. - Rat Genome Database

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Regional differential expression of TREK-1 at left ventricle in myocardial infarction.

Authors: Zhao, LN  Fu, L  Gao, QP  Xie, RS  Cao, JX 
Citation: Zhao LN, etal., Can J Cardiol. 2011 Nov-Dec;27(6):826-33. doi: 10.1016/j.cjca.2011.01.013. Epub 2011 Jun 16.
RGD ID: 9831182
Pubmed: PMID:21683547   (View Abstract at PubMed)
DOI: DOI:10.1016/j.cjca.2011.01.013   (Journal Full-text)

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.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
myocardial infarction  ISOKcnk2 (Rattus norvegicus)9831182; 9831182mRNA:decreased expression:heart left ventricle more ...RGD 
myocardial infarction  IEP 9831182mRNA:decreased expression:heart left ventricle more ...RGD 

Objects Annotated

Genes (Rattus norvegicus)
Kcnk2  (potassium two pore domain channel subfamily K member 2)

Genes (Mus musculus)
Kcnk2  (potassium channel, subfamily K, member 2)

Genes (Homo sapiens)
KCNK2  (potassium two pore domain channel subfamily K member 2)


Additional Information