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

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^*

^*Corresponding author for this work

Medicine, Cardiology Division

Research output: Contribution to journal › Article

3 Scopus citations

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)
Pages (from-to)	405-410
Number of pages	6
Journal	Journal of Molecular and Cellular Cardiology
Volume	44
Issue number	2
DOIs	https://doi.org/10.1016/j.yjmcc.2007.10.014
State	Published - Feb 2008

Keywords

Calmodulin kinase II
Cardiomyopathy
eGFP

ASJC Scopus subject areas

Molecular Biology
Cardiology and Cardiovascular Medicine

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Khoo, M. S. C., Grueter, C. E., Eren, M., Yang, J., Zhang, R., Bass, M. A., Lwin, S. T., Mendes, L. A., Vaughan, D. E., Colbran, R. J., & Anderson, M. E. (2008). Calmodulin kinase II inhibition disrupts cardiomyopathic effects of enhanced green fluorescent protein. Journal of Molecular and Cellular Cardiology, 44(2), 405-410. https://doi.org/10.1016/j.yjmcc.2007.10.014

Khoo, Michelle S C ; Grueter, Chad E. ; Eren, Mesut ; Yang, Jinying ; Zhang, Rong ; Bass, Martha A. ; Lwin, Seint T. ; Mendes, Lisa A. ; Vaughan, Douglas E. ; Colbran, Roger J. ; Anderson, Mark E. / Calmodulin kinase II inhibition disrupts cardiomyopathic effects of enhanced green fluorescent protein. In: Journal of Molecular and Cellular Cardiology. 2008 ; Vol. 44, No. 2. pp. 405-410.

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title = "Calmodulin kinase II inhibition disrupts cardiomyopathic effects of enhanced green fluorescent protein",

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.",

keywords = "Calmodulin kinase II, Cardiomyopathy, eGFP",

author = "Khoo, {Michelle S C} and Grueter, {Chad E.} and Mesut Eren and Jinying Yang and Rong Zhang and Bass, {Martha A.} and Lwin, {Seint T.} and Mendes, {Lisa A.} and Vaughan, {Douglas E.} and Colbran, {Roger J.} and Anderson, {Mark E.}",

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Calmodulin kinase II inhibition disrupts cardiomyopathic effects of enhanced green fluorescent protein. / Khoo, Michelle S C; Grueter, Chad E.; Eren, Mesut; Yang, Jinying; Zhang, Rong; Bass, Martha A.; Lwin, Seint T.; Mendes, Lisa A.; Vaughan, Douglas E.; Colbran, Roger J.; Anderson, Mark E.

In: Journal of Molecular and Cellular Cardiology, Vol. 44, No. 2, 02.2008, p. 405-410.

Research output: Contribution to journal › Article

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AU - Khoo, Michelle S C

AU - Grueter, Chad E.

AU - Eren, Mesut

AU - Yang, Jinying

AU - Zhang, Rong

AU - Bass, Martha A.

AU - Lwin, Seint T.

AU - Mendes, Lisa A.

AU - Vaughan, Douglas E.

AU - Colbran, Roger J.

AU - Anderson, Mark E.

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AB - 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.

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