Calmodulin kinase II inhibition disrupts cardiomyopathic effects of enhanced green fluorescent protein

Michelle S.C Khoo; Chad E Grueter; Mesut Eren; Jinying Yang; Rong Zhang; Martha A Bass; Seint T Lwin; Lisa A Mendes; Douglas E Vaughan; Roger J Colbran; Mark E Anderson

doi:10.1016/j.yjmcc.2007.10.014

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Calmodulin kinase II inhibition disrupts cardiomyopathic effects of enhanced green fluorescent protein

Journal article

Peer reviewed

Calmodulin kinase II inhibition disrupts cardiomyopathic effects of enhanced green fluorescent protein

Michelle S.C Khoo, Chad E Grueter, Mesut Eren, Jinying Yang, Rong Zhang, Martha A Bass, Seint T Lwin, Lisa A Mendes, Douglas E Vaughan, Roger J Colbran, …

Journal of molecular and cellular cardiology, Vol.44(2), pp.405-410

02/2008

DOI: 10.1016/j.yjmcc.2007.10.014

PMCID: PMC2695824

PMID: 18048055

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Abstract

Transgenic expression of enhanced green fluorescent protein (eGFP) in myocardium can result in cardiac dysfunction and cardiomyopathy, presumably through toxic effects that disrupt normal cellular signaling. The multifunctional Ca2+- and calmodulin-dependent protein kinase II (CaMKII) is widely expressed in myocardium and CaMKII activity is increased in human and animal models of cardiomyopathy, so we hypothesized that increased CaMKII activity is important for cardiomyopathy due to transgenic expression of eGFP. Here we report that cardiomyocyte-delimited eGFP over-expression causes increased CaMKII activity that predicts left ventricular dilation and dysfunction. On the other hand, transgenic co-expression of a CaMKII inhibitory peptide with eGFP prevents eGFP-mediated left ventricular dilation and dysfunction. These findings suggest that increased CaMKII activity is a critical pathological signal in transgenic cardiomyopathy due to eGFP over-expression.

Calmodulin kinase II

Cardiomyopathy

eGFP

Details

Title: Subtitle: Calmodulin kinase II inhibition disrupts cardiomyopathic effects of enhanced green fluorescent protein
Creators: Michelle S.C Khoo - Department of Internal Medicine, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045, USA
Chad E Grueter - Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232, USA
Mesut Eren - Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232, USA
Jinying Yang - Department of Internal Medicine, Carver College of Medicine, University of Iowa, IA 52240, USA
Rong Zhang - Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232, USA
Martha A Bass - Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN 37232, USA
Seint T Lwin - Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232, USA
Lisa A Mendes - Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232, USA
Douglas E Vaughan - Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232, USA
Roger J Colbran - Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN 37232, USA
Mark E Anderson - Department of Internal Medicine, Carver College of Medicine, University of Iowa, IA 52240, USA
Resource Type: Journal article
Publication Details: Journal of molecular and cellular cardiology, Vol.44(2), pp.405-410
DOI: 10.1016/j.yjmcc.2007.10.014
PMID: 18048055
PMCID: PMC2695824
NLM abbreviation: J Mol Cell Cardiol
ISSN: 0022-2828
eISSN: 1095-8584
Publisher: Elsevier Ltd
Language: English
Date published: 02/2008
Academic Unit: Cardiovascular Medicine; Craniofacial Anomalies Research Center; Internal Medicine
Record Identifier: 9984094316102771

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