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 language | English (US) |
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Pages (from-to) | 405-410 |
Number of pages | 6 |
Journal | Journal of Molecular and Cellular Cardiology |
Volume | 44 |
Issue number | 2 |
DOIs | |
State | Published - Feb 2008 |
Keywords
- Calmodulin kinase II
- Cardiomyopathy
- eGFP
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine