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Long‐term restitution of 4‐aminopyridine‐sensitive currents in Kv1DN ventricular myocytes using adeno‐associated virus‐mediated delivery of Kv1.5
Author(s) -
Kodirov S.A,
Brunner M,
Busconi L,
Koren G
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)00822-6
Subject(s) - myocyte , 4 aminopyridine , adeno associated virus , chemistry , potassium channel , microbiology and biotechnology , recombinant dna , medicine , biophysics , virology , vector (molecular biology) , biology , gene , biochemistry
Overexpression of a dominant‐negative truncated Kv1.1 (Kv1DN) polypeptide in the mouse heart resulted in marked attenuation of a 4‐aminopyridine (4‐AP)‐sensitive current, I K,slow1 . We used recombinant adeno‐associated virus (rAAV) as a vector for direct delivery of Kv1.5 into the mouse myocardium in order to normalize the action potential duration (APD) 6 months after injection. The injection of rAAV‐Kv1.5 reconstituted the 4‐AP‐sensitive outward potassium currents, shortened the APD, and eliminated spontaneous early afterdepolarizations. Immunoblots detected the FL‐Kv1.5 polypeptides only in rAAV‐Kv1.5‐infected hearts. These data demonstrate long‐term expression of 4‐AP‐sensitive potassium currents in ventricular myocytes by gene transfer using rAAV vector encodes Kv1.5.