NDLI: Basal and IGF-I-dependent regulation of potassium channels by MAP kinases and PI3-kinase during eccentric cardiac hypertrophy

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Teos, Leyla Y. Zhao, Aiqiu Alvin, Zikiar Laurence, Graham G. Li, Chuanfu Haddad, Georges E.
Description	Country affiliation: United States Author Affiliation: Teos LY ( Department of Physiology and Biophysics, College of Medicine, Howard University, Washington, DC 20059, USA.)
Abstract	The potassium channels $I_{K}$ and $I_{K1},$ responsible for the action potential repolarization and resting potential respectively, are altered during cardiac hypertrophy. The activation of insulin-like growth factor-I (IGF-I) during hypertrophy may affect channel activity. The aim was to examine the modulatory effects of IGF-I on $I_{K}$ and $I_{K1}$ through mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways during hypertrophy. With the use of specific inhibitors for ERK1/2 (PD98059), p38 MAPK (SB203580) and PI3K/Akt ({"type":"entrez-nucleotide","attrs":{"text":"LY294002","term_id":"1257998346","term_text":"LY294002"}}LY294002), Western blot and whole cell patch-clamp were conducted on sham and aorto-caval shunt-induced hypertrophy adult rat myocytes. Basal activation levels of MAPKs and Akt were increased during hypertrophy. Acute IGF-I $(10^{−8}$ M) enhanced basal activation levels of these kinases in normal hearts but only those of Akt in hypertrophied ones. $I_{K}$ and $I_{K1}$ activities were lowered by IGF-I. Inhibition of ERK1/2, p38 MAPK, or Akt reduced basal $I_{K}$ activity by 70, 32, or 50%, respectively, in normal cardiomyocytes vs. 53, 34, or 52% in hypertrophied ones. However, basal activity of $I_{K1}$ was reduced by 45, 48, or 45% in the former vs. 63, 43, or 24% in the latter. The inhibition of either MAPKs or Akt alleviated IGF-I effects on $I_{K}$ and $I_{K1}.$ We conclude that basal $I_{K}$ and $I_{K1}$ are positively maintained by steady-state Akt and ERK activities. $K^{+}$ channels seem to be regulated in a dichotomic manner by acutely stimulated MAPKs and Akt. Eccentric cardiac hypertrophy may be associated with a change in the regulation of the steady-state basal activities of $K^{+}$ channels towards MAPKs, while that of the acute IGF-I-stimulated ones toward Akt.
File Format	HTM / HTML
ISSN	03636135
e-ISSN	15221539
DOI	10.1152/ajpheart.321.2008
Journal	AJP: Heart and Circulatory Physiology
Issue Number	5
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Cardiology Cardiomegaly Enzymology Insulin-like Growth Factor I Metabolism Mitogen-activated Protein Kinases Myocytes, Cardiac Phosphatidylinositol 3-kinases Potassium Channels Signal Transduction Animals Disease Models, Animal Membrane Potentials Mitogen-activated Protein Kinase 1 Mitogen-activated Protein Kinase 3 Antagonists & Inhibitors Drug Effects Phosphorylation Protein Kinase Inhibitors Pharmacology Proto-oncogene Proteins C-akt Rats, Sprague-dawley Time Factors P38 Mitogen-activated Protein Kinases Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Cardiology and Cardiovascular Medicine

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