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Cardiovascular Research 1998 37(2):360-366; doi:10.1016/S0008-6363(97)00270-8
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Sarcoplasmic reticulum Ca2+-ATPase overexpression by adenovirus mediated gene transfer and in transgenic mice

Markus Meyer and Wolfgang H Dillmann*

Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0618, USA

* Corresponding author. Tel. (+1-619) 534 9934; Fax (+1-619) 534 9932; E-mail: wdillman@ucsd.edu

The sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) is a major determinant of cardiac relaxation. It has been demonstrated that the steady state levels of the mRNA coding for this pump are reduced in human heart failure due to dilated cardiomyopathy. Although results regarding the protein level are controversial, most functional studies indicate decreased SERCA2a activity in heart failure. The extent to which a potential decrease in the calcium sequestering function of this protein could contribute to the contractile dysfunction in heart failure, and whether a reconstitution of SERCA2a could alleviate heart failure, are yet unknown. To further investigate these questions two methodological approaches were chosen. Adenovirus mediated gene transfer provides an approach to study functional consequences of SERCA2a overexpression in cardiac myocytes in vitro [1], and a transgenic mouse model allows the effects of cardiac overexpression of SERCA2a to be examined in vivo [2].

KEYWORDS Sarcoplasmic reticulum Ca2+-ATPase; Adenovirus; Transgenic mice; Cardiac contractility; Relaxation; Calcium transients


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