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

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)405-410
Number of pages6
JournalJournal of Molecular and Cellular Cardiology
Volume44
Issue number2
DOIs
StatePublished - Feb 2008
Externally publishedYes

Keywords

  • Calmodulin kinase II
  • Cardiomyopathy
  • eGFP

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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