Long-term restitution of 4-aminopyridine-sensitive currents in Kv1DN ventricular myocytes using adeno-associated virus-mediated delivery of Kv1.5

S. A. Kodirov; M. Brunner; L. Busconi; G. Koren

doi:10.1016/S0014-5793(03)00822-6

Long-term restitution of 4-aminopyridine-sensitive currents in Kv1DN ventricular myocytes using adeno-associated virus-mediated delivery of Kv1.5

S. A. Kodirov, M. Brunner, L. Busconi, G. Koren

Research output: Contribution to journal › Article › peer-review

36 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	74-78
Number of pages	5
Journal	FEBS Letters
Volume	550
Issue number	1-3
DOIs	https://doi.org/10.1016/S0014-5793(03)00822-6
State	Published - 28 Aug 2003
Externally published	Yes

Keywords

4-Aminopyridine
Adeno-associated virus
Delayed rectifier K channel

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10.1016/S0014-5793(03)00822-6

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title = "Long-term restitution of 4-aminopyridine-sensitive currents in Kv1DN ventricular myocytes using adeno-associated virus-mediated delivery of Kv1.5",

abstract = "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, IK,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.",

keywords = "4-Aminopyridine, Adeno-associated virus, Delayed rectifier K channel",

author = "Kodirov, {S. A.} and M. Brunner and L. Busconi and G. Koren",

note = "Funding Information: The support of grants from The National Institutes of Health is gratefully acknowledged. We wish to thank Dr. R. Mulligan and Dr. Jeng-Shin Lee, Harvard Gene Therapy Initiative, for the preparation of the rAAV-vectors and Jun Zhou for his comments.",

year = "2003",

month = aug,

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doi = "10.1016/S0014-5793(03)00822-6",

language = "אנגלית",

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pages = "74--78",

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T1 - Long-term restitution of 4-aminopyridine-sensitive currents in Kv1DN ventricular myocytes using adeno-associated virus-mediated delivery of Kv1.5

AU - Kodirov, S. A.

AU - Brunner, M.

AU - Busconi, L.

AU - Koren, G.

N1 - Funding Information: The support of grants from The National Institutes of Health is gratefully acknowledged. We wish to thank Dr. R. Mulligan and Dr. Jeng-Shin Lee, Harvard Gene Therapy Initiative, for the preparation of the rAAV-vectors and Jun Zhou for his comments.

PY - 2003/8/28

Y1 - 2003/8/28

N2 - 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, IK,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.

AB - 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, IK,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.

KW - 4-Aminopyridine

KW - Adeno-associated virus

KW - Delayed rectifier K channel

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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

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