Abstract：
:Rhythmic cardiac contractions depend on the organized propagation of depolarizing and repolarizing wavefronts. Repolarization is spatially heterogeneous and depends largely on gradients of potassium currents. Gradient disruption in heart disease may underlie susceptibility to fatal arrhythmias, but it is not known how this gradient is established. We show that, in mice lacking the homeodomain transcription factor Irx5, the cardiac repolarization gradient is abolished due to increased Kv4.2 potassium-channel expression in endocardial myocardium, resulting in a selective increase of the major cardiac repolarization current, I(to,f), and increased susceptibility to arrhythmias. Myocardial Irx5 is expressed in a gradient opposite that of Kv4.2, and Irx5 represses Kv4.2 expression by recruiting mBop, a cardiac transcriptional repressor. Thus, an Irx5 repressor gradient negatively regulates potassium-channel-gene expression in the heart, forming an inverse I(to,f) gradient that ensures coordinated cardiac repolarization while also preventing arrhythmias.
journal_name
Celljournal_title
Cellauthors
Costantini DL,Arruda EP,Agarwal P,Kim KH,Zhu Y,Zhu W,Lebel M,Cheng CW,Park CY,Pierce SA,Guerchicoff A,Pollevick GD,Chan TY,Kabir MG,Cheng SH,Husain M,Antzelevitch C,Srivastava D,Gross GJ,Hui CC,Backx PH,Bruneaudoi
10.1016/j.cell.2005.08.004subject
Has Abstractpub_date
2005-10-21 00:00:00pages
347-58issue
2eissn
0092-8674issn
1097-4172pii
S0092-8674(05)00807-Xjournal_volume
123pub_type
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